|تعداد مشاهده مقاله||111,536,312|
|تعداد دریافت فایل اصل مقاله||86,168,763|
Effects of Hesperidin During Pregnancy on Antidepressant-like behaviour in Postpartum Mice
|Iranian Journal of Veterinary Medicine|
|دوره 14، شماره 3، آبان 2020، صفحه 261-270 اصل مقاله (435.25 K)|
|نوع مقاله: Physiology|
|شناسه دیجیتال (DOI): 10.22059/ijvm.2020.297314.1005062|
|Ava Khodadadeh1؛ Shahin Hassanpour* 2؛ Ghasem Akbari3|
|1Graduated from the Faculty of Veterinary Medicine, Science and Research Branch, Islamic Azad University, Tehran, Iran|
|2Division of Physiology, Department of Basic Sciences, Faculty of Veterinary Medicine, Science and Research Branch, Islamic Azad University, Tehran, Iran|
|3Department of Clinical Sciences, Faculty of Veterinary Medicine, Science and Research Branch, Islamic Azad University, Tehran, Iran|
|BACKGROUND:Post-partum depression is the most prevalent form of mental illness and herbal therapies are potential alternatives and adjuncts for its treatment. Hesperidin is the major flavonoid isolated from cit- rus fruits which has neuroprotective, antioxidant and antidepressant activity.|
OBJECTIVES: We studied the effect of exposure to Hesperidin during pregnancy on postpartum antide- pressant-like effects in mice.
METHODS: Twelve male and 40 female mice (28-30 gr) were randomly selected and after determina- tion of the pregnancy using vaginal plaque, allocated into 4 experimental groups. Group 1 was kept as control and groups 2-4 were i.p. injected with 0.1, 0.5 and 1 mg/kg of hesperidin on days of 5, 8, 11, 14 and 17 of pregnancy. The control group received i.p. injection of the saline on the same days. Following postpartum, forced swimming test (FST), tail suspension test (TST) and open field tests were used to eval- uate depressive-like antidepressant activity of hesperidin. At the end of the study, serum Malondialde- hyde (MDA), glutathione peroxidase (GPx), superoxide dismutase (SOD) and total antioxidant capacity (TAC) were determined.
RESULTS: According to the results, administration of the different levels of the hesperidin (0.5 and 1 mg/ kg) at GD 5, 8, 11, 14 and 17 significantly decreased immobility time (S) in TST and FST on postpartum mice compared to control group (p ≤0.05). Pre-partum administration of hesperidin (0.1, 0.5 and 1 mg/kg) had no significant effect on OFT of control group (p >0.05). Administration of the hesperidin (0.5 and 1 mg/ kg) during the GD significantly decreased MDA levels on postpartum compared to control group (p ≤0.05). Also, pre-partum administration of the hesperidin (0.1, 0.5 and 1 mg/kg) significantly increased SOD and GPx levels on postpartum mice compared to control group (p ≤0.05).
CONCLUSIONS: These results suggested pre-partum administration of hesperidin has antidepressant and antioxidant effect in postpartum mice.
|Pregnancy؛ Hesperidin؛ Antidepressant؛ Antioxidant؛ Postpartum؛ Mice|
|عنوان مقاله [English]|
|اثرات تجویز هیسپیریدین طی دوران آبستنی بر رفتار ضدافسردگی پس از زایمان در موش سوری|
|آوا خداداده1؛ شاهین حسن پور2؛ قاسم اکبری3|
|1دانش آموخته دکتری عمومی دامپزشکی، دانشکده دامپزشکی، واحد علوم و تحقیقات، دانشگاه آزاد اسلامی، تهران، ایران|
|2بخش فیزیولوژی، گروه علوم پایه، دانشکده دامپزشکی، واحد علوم و تحقیقات، دانشگاه آزاد اسلامی، تهران، ایران|
|3گروه علوم درمانگاهی، دانشکده دامپزشکی، واحد علوم و تحقیقات، دانشگاه آزاد اسلامی، تهران، ایران|
|زمینه مطالعه: افسردگی پس از زایمان یکی از شایعترین بیماریهای روان میباشد و درمان گیاهی جایگزین مناسبی برای درمان آن میباشد. هیسپریدین مهمترین فلاوونوئید استخراج شده از مرکبات میباشد که اثرات محافظتی بر نورون، آنتی اکسیدانی و ضد افسردگی دارد. |
هدف: مطالعه حاضر به منظور بررسی اثرات قرار گرفتن در معرض هیسپریدین در دوران آبستنی بر اثرات ضدافسردگی متعاقب زایمان در موشهای سوری انجام گرفت.
روش کار: 12 موش سوری نر و 40 موش ماده بالغ (28-30 گرم) بطور تصادفی در کنار یکدیگر نگهداری شده و پس از تایید آبستنی بوسیله پلاک واژن، به چهار گروه تقسیم شدند. گروه اول بعنوان کنترل و گروه 2، 3 و 4 به ترتیب تزریق 1/0، 5/0 و 1 گرم بر کیلوگرم هیسپریدین را طی روزهای 5، 8، 11، 14 و 17 آبستنی را بصورت تزریق داخل صفاقی دریافت کردند. به گروه کنترل نیز در همان فواصل سرم فیزیولوژی تزریق شد. پس از زایمان ارزیابی اثرات ضدافسردگی هیسپیریدین با استفاده از آزمونهای شنای اجباری، تعلیق دم و اوپن فیلد انجام گرفت. در انتهای مطالعه، نمونه خون اخذ و مقادیر سرمی مالون دی آلدهید (MDA)، گلوتاتیون پراکسیداز (GPx)، سوپرااکسید دیسموتاز (SOD) و ظرفیت آنتی اکسیدانی تام (TAC) ارزیابی شد.
نتایج: باتوجه به نتایج بدست آمده تجویز هیسپریدین (1/0، 5/0 و 1 گرم بر کیلوگرم) طی روزهای 5، 8، 11، 14 و 17 آبستنی بطور معنیداری موجب کاهش زمان بیتحرکی (ثانیه) در تستهای شنای اجباری و تعلیق دم متعاقب زایمان در مقایسه با گروه کنترل شد (05/0≥p < /em>). تجویز هیسپریدین (1/0، 5/0 و 1 گرم بر کیلوگرم) طی روزهای 5، 8، 11، 14 و 17 آبستنی بطور اثر معنیداری در تست اپن فیلد در مقایسه با گروه کنترل نداشت(05/0<p < /em>). تجویز هیسپریدین (1/0، 5/0 و 1 گرم بر کیلوگرم) طی آبستنی موجب کاهش مالون دی آلدهید متعاقب زایمان در مقایسه با گروه کنترل شد (05/0≥p < /em>). همچنین، تجویز هیسپریدین (1/0، 5/0 و 1 گرم بر کیلوگرم) در دوران آبستنی موجب افزایش گلوتاتیون پراکسیداز و سوپرااکسید دیسموتاز در مقایسه با گروه کنترل شد (05/0≥p < /em>).
نتیجه گیری نهایی: نتایج نشان دهنده این بود که قرار گرفتن در تجویز هیسپریدین در دوران آبستنی اثرات ضدافسردگی و آنتی اکسیدانی متعاقب زایمان در موش سوری دارد.
|هیسپیریدین, ضدافسردگی, آنتی اکسیدان, زایمان, موش|
Depressive disorders are the most preva- lent form of mental illness worldwide. Major depression is characterized by a change in psychosocial and physical impairment mood as well as lack of interest in the surroundings (Saravi et al., 2016). There are growing re- ports on the incidence of depression in both males and females that imposes a substantial health burden on society (Gu et al., 2014). The post-partum period represents profound physiological and emotional changes in mothers to ensure the well-being and nurtur- ance of the offspring. However, several psy- chiatric disorders can develop in this phase (Perani and Slattery, 2014). Post-partum mood and anxiety disorders affect maternal and infant as well as developing psychiat- ric disorder in later life such as post-partum depression (PPD), post-partum anxiety and post-partum psychosis (Ming and Shinn- Yi, 2016). Several animal methods such as stress-based, high-fat diet-based and pup separation models are used to induce exper- imental PPD (Ming and Shinn-Yi, 2016). There are growing reports of new antide- pressant agents to provide clinically relevant perceptions into the neuropathology that un- derlies the idiopathic disease state of depres- sion (Alimohammadi et al., 2019).
Hesperidin is the major flavonoid isolated from citrus fruits (Li and Schluesener, 2017). The hesperidin molecule is composed of a glycone unit known as hesperetin and a di- saccharide, rutinose (Iranshahi et al., 2015). Hesperidin has several biological effects including antioxidant, anti-inflammatory, antimicrobial, anti-carcinogenic and anti-al- lergic effects and insulin-sensitizing activ- ity (Li and Schluesener, 2017). In addition, hesperidin neuropharmacological properties have been reported for the hesperidin (Ha-
jialyani et al., 2019). It has high potential for radical scavenging and protective effects and can cross blood brain barrier (Khan and Parvez, 2015). Hesperidin promotes neuro- nal survival, differentiation and neuropro- tective capacity of astrocytes (Matias et al., 2017) which have positive effect for stroke, Huntington’s, Alzheimer’s and Parkinson’s disease (Antunes et al., 2014). Several an- tioxidant compounds, such as flavonoids derived from natural products, have demon- strated neuroprotective activity in PPD (An- tunes et al., 2014).
Antioxidant enzymes, such as glutathione peroxidase (GPx), catalase (CAT) and super- oxide dismutase (SOD), also are important mediators in the reduction of oxidative stress (Khan et al. 2012). It is reported that (50 mg/ kg) treatment increased GPx, SOD and CAT activity in mouse model of Parkinson’s dis- ease (Antunes et al., 2014). Hesperidin in the acute (1 mg/kg) and chronic (0.1, 0.3 and 1 mg/kg) levels improved tail suspension test (TST) which improved antidepressant-like effect (Donato et al., 2014). Based on the aforementioned evidence, we sought to in- vestigate effects of the Hesperidin exposure during pregnancy on antidepressant-like ef- fects postpartum in mice.
Materials and methods
The NMRI male (n=12) and virgin female mice (n=40, age: 8–10 weeks old and 28–30 gr) were supplied from the Razi Serum and Vaccine Institute (Tehran, Iran). The animals were kept five mice/cage in standard plastic cages at laboratory conditions (temperature of 22 ± 2 °C and 12/h light/dark cycle) with ad libitum access to standard chow pellet (Pars Dam Co, Tehran, Iran) and fresh wa-
ter. The animals acclimatized for 1 week before beginning the study. All experimen- tal procedures were approved by the Animal Ethics Committee of Science and Research Branch of Islamic Azad University, Tehran, Iran (IR.IAU.SRB.REC.1398.117) following the Guidelines for the Care and Use of Lab- oratory Animals in Research. After 1 week of acclimatization, the female mice were caged with fertile male mice. Each morning, the fe- male mice were examined for the presence of sperm or vaginal plug. Presence of the vaginal plug or sperm was defined as onset of preg- nancy. The pregnant mice were randomly as- signed into 4 groups (n = 10 for each group) and provided ad libitum food and water.
Hesperidin (H5254) was purchased from Sigma Aldrich, (Saint Luis, USA) and were dissolved by the sequential addition of di- methyl sulfoxide up to a final concentration of 5%, a water solution of 0.25% Tween 80 up to a final concentration of 20% and saline to complete 100% volume (Donato et al., 2014).
In control group, pregnant mice were
i.p. injected with saline containing 0.05% Tween-80 at gestation day (GD) 5, 8, 11, 14 and 17. In groups 2, 3 and 4, mice were in- jected with 0.1, 0.5 and 1 mg/kg of hesper- idin at GD 5, 8, 11, 14 and 17, respectively. The dosage of the hesperidin was determined based on the previous reports (Antunes et al., 2014; Donato et al., 2014; Khan and Parvez, 2015; Pari et al., 2015) and our pilot study. Then after delivery, antidepressant-like ef- fects of the hesperidin were evaluated using neurobehavioral tests that were done on fe- male mice.
Tail suspension test (TST)
The TST is one of the most common tech- niques for assessing antidepressant-like ac-
tivity in mice (Cryan et al., 2005). The TST was done based on the method stated by Ste- ru et al. (1985). Briefly, the mice were far from nearest objects and were both acousti- cally and visually isolated from observing or interacting each other. Each mouse was then suspended 50 cm above the floor by adhesive tape placed approximately 1 cm from the ex- tremity of the tail, in such a position that it cannot escape or hold on to nearby surfac- es. Immobility time was recorded during a
6 min period. Mice were considered im- mobile only when they had no strong body shaking and movement of the limbs as they hung passively and completely motionless.
Open field test (OFT)
The Open field test (OFT) was used to determine possible effects of hesperidin on the locomotor and exploratory activities. The OFT was done using 45×45×30 cm3 poly wood cage. The flour of OFT cage was divided by masking tape markers into 3×3 squares. Each animal was placed individual- ly at the center of the apparatus and observed for 6 min to record the locomotion (number of segments crossed with the four paws) (Donato et al., 2014).
Forced Swimming Test (FST)
FST was carried out following the protocol as described previously in mice (Castagné et al., 2011). Each mouse was plunged into a glass cylinder (height: 25 cm; diameter: 15 cm) containing 10 cm of water (25 ± 1 °C) for 15 min (pre-test session). Twenty-four hours later, the mouse was placed in the cyl- inder again and left for a 6 min period (test session). The immobility time for mouse was described as when it ceased struggling and remained floating motionless in the water, making only small movements necessary to keep its head above water. The total duration of immobility during the last 4 min of the 6
min testing period was measured.
At the end of the neurobehavioral tests, blood samples were taken from each mouse and serum Malondialdehyde (MDA), SOD, GPx and total antioxidant capacity (TAC) were determined using Zell Bio GmbH (Germany) assay kits (ZB-MDA-48A, ZB-SOD-A48, ZB-
GPX-A48 and ZB-TAC-48A, respectively).
Data was analyzed by one-way analysis of variance (ANOVA) and is presented as the mean ± SEM. For treatments found to have an effect according to the ANOVA, mean
values were compared with Tukey’s test. P≤0.05 was considered to indicate signifi- cant differences between the treatments.
Effect of exposure to different levels of Hes- peridin during pregnancy on immobility time
(S) in TST on postpartum mice is presented in Figure 1. As seen, administration of the differ- ent levels of the hesperidin (0.5 and 1 mg/kg) at GD 5, 8, 11, 14 and 17 significantly decreased immobility time (s) in TST on postpartum mice compared to control group (P≤0.05).
Figure 1. Effect of exposure to different levels of Hesperidin during pregnancy on immo- bility time (sec) in TST on postpartum mice. TST: tail suspension test. There are signifi- cant differences between groups with different superscripts (a, b and c; P ≤ 0.05).
According to the Figure 2, administra- tion of the hesperidin (0.5 and 1 mg/kg) at GD 5, 8, 11, 14 and 17 significantly
decreased immobility time (S) in FST on postpartum mice compared to control group (P≤0.05).
Figure 2. Effect of exposure to different levels of Hesperidin during pregnancy on immo- bility time (sec) in FST on postpartum mice. FST: forced swimming test. There are signifi- cant differences between groups with different superscripts (a, b and c; P ≤ 0.05).
However, pre-partum exposure to the hes- peridin (0.1, 0.5 and 1 mg/kg) had no signif-
icant effect on OFT following delivery com- pared to control group (P>0.05) (Figure 3).
Figure 3. Effect of exposure to different levels of Hesperidin during pregnancy on im- mobility time (S) in OFT on postpartum mice. OFT: open field test.
As seen in Figure 4. administration of the hesperidin (0.5 and 1 mg/kg) during the GD significantly decreased MDA levels on postpartum mice compared to control group
(P≤0.05). Furthermore, administration of the hesperidin (0.5 and 1 mg/kg) significantly in- creased GPx levels on postpartum mice com- pared to control group (P≤0.05) (Figure 5).
Figure 4. Effect of exposure to different levels of Hesperidin during pregnancy on postpartum serum Malondialdehyde (MDA) level n mice. There are significant differences between groups with different superscripts (a and b; P ≤ 0.05).
Figure 5. Effect of exposure to different levels of Hesperidin during pregnancy on postpartum serum glutathione peroxi- dase (GPx) level in mice. There are significant differences between groups with different superscripts (a and b; P ≤ 0.05).
Pre-partum exposure to the hesperidin (0.1,
0.5 and 1 mg/kg) significantly increased SOD levels on postpartum mice compared to control
group (P≤0.05) (Figure 6) but had no signif- icant effect on TAC following delivery com- pared to control group (P>0.05) (Figure 7).
Figure 6. Effect of exposure to different levels of Hesperidin during pregnancy on postpartum serum superoxide dismutase (SOD) level in mice. There are significant differences between groups with different superscripts (a and b; P ≤ 0.05).
Figure 7. Effect of exposure to different levels of Hesperidin during pregnan- cy on postpartum serum total antioxidant capacity (TAC) in mice.
postpartum mice compared to control group.
Depression is a common, chronic, recur- rent illness with severe morbidity. Although a number of research studies have been done on its physiological mechanisms, brain areas underlying this disorder are not yet well un- derstood. Postpartum depression is a severe mood disorder which happens right away after childbirth and is observed by sadness and anx- iety in mothers (O'Hara and McCabe, 2013). According to the results, administration of the different doses of hesperidin (0.5 and 1 mg/ kg) at GD 5, 8, 11, 14 and 17 significantly de- creased immobility time in TST and FST on
Hesperidin (1mg/kg) significantly reduced immobility time in FST in mice (Filho et al., 2013). In a similar study, it was reported hes- peridin (50 mg/kg) improved depressive-like behavior in the TST and memory in the Mor- ris water maze test (Antunes et al., 2014). The antidepressant-like effect of hesperidin has been reported in FST and TST tests (Souza et al., 2013). Moreover, hesperidin suppressed depressive-like behaviors in TST using in- tra-striatal injection of 6-hydroxydopamine in Parkinson's disease (Antunes et al., 2014). Hesperidin (25, 50 and 100 mg/kg) had an- ti-depressant effect in diabetic rats (El-Mara-
sy et al., 2014), our results were in agreement with the reports.
Immobility time in FST resembles a state of despair and mental depression. Stress-in- duced depression like behavioral alterations are routinely determined by TST and FST in rodents. Immobility time in TST and FST reflects the behavioral despair which is sim- ilar to depression in human (Walia and Gil- hotra, 2016). Differences on neurochemical pathways of the FST and TST induced per- formance are reported/have been reported. At face value, these two tests appear very simi- lar but this potency difference appears due to both pharmacokinetic and pharmacodynamic factors (Amin et al., 2015). We also studied effect of the hesperidin on locomotor activity using open field test. AS observed, pre-par- tum exposure to the hesperidin (0.1, 0.5 and 1 mg/kg) had no significant effect on OFT following delivery. It is revealed hesperidin at the levels of 0.1, 0.5 and 1 mg/kg, had no sedative effect, our finding was similar to this report.
Bioavailability is a key step in ensuring the bio efficacy of hesperidin which is affected by physiological conditions. It is selectively me- tabolized by both cytochrome P450 isoforms (CYP1A and CYP1B1) to eriodictyol, indicat- ing that there is Odemethylation of hesperidin in liver. It has higher bio activity compared to the other flavonoids which can be related to the inhibition of phase II metabolism (glucu- ronidation and sulfation of hesperidin). The metabolites of hesperidin are detected in urine but not in feces. In oral administration, more than 40% of the radioactivity of hesperidin
-3-14C was expired as carbon dioxide which indicates further bacterial degradation in the colon than blood circulation (Roohbakhsh et al., 2014). The ability of hesperidin to cross the blood brain barrier makes it an ideal bio-
active substance for treatment of CNS dis- orders (Iranshahi et al., 2015). Hesperidin decreases risk of Parkinson's disease as well as Alzheimer's disease in flavonoid deficient patient (Antuneset al., 2014). The neuropro- tective role of the hesperidin is mediated via anti-inflammatory and antioxidant activities (Menze et al., 2012). Hesperidin (0.01, 0.3 and 1 mg/kg) has antidepressant-like effect in TST and decreased nitrate/nitrite as well as increased hippocampal brain-derived neu- rotrophic factor (BDNF) in the hippocampus of mice (Donato et al., 2014). Based on lit- erature, NO/cGMP pathway has a key role on antidepressant effect of hesperidin (Do- nato et al., 2014). It is reported that nitrate/ nitrite levels decreased in the hippocampus of hesperidin-treated mice. Anti-depressant activity of the hesperidin is inhibited by pre- treatment with L-arginine (processor of nitric oxide). Also, administration of the hesperidin increased the brain-derived neurotrophic fac- tor (BDNF) level in the hippocampus of mice (Donato et al., 2014). Perhaps, antidepres- sant-like activity of the flavonoids mediates via BDNF (Hajialyani et al., 2019). Also, it is reported antidepressant effect of hesperidin is also dependent on nitric oxide (NO)/cGMP pathway (Donato et al., 2014). Hesperidin, acute (1 mg/kg) and chronic (0.1, 0.3 and 1 mg/kg), reduced nitrate/nitrite levels in the hippocampus of mice (Donato et al. 2014). However, the mechanisms and brain areas underlying the pathophysiology of depression are not fully elicited. It is suggested plasma nitrate levels and nitric oxide synthase (NOS) expression increased in the hippocampus of depressed patients. Inhibition of NOS may decrease immobility time in the TST elicited by hesperidin (Donato et al., 2014). Based on the limitation of the study, we were not able to determine interaction of the hesperi-
din with NO pathway.
Based on the findings, pre-partum exposure to the hesperidin (0.1, 0.5 and 1 mg/kg) signifi- cantly increased SOD and GPx levels on post- partum mice compared to control group. It is reported that hesperidin has antioxidant pro- tection against free radicals-induced oxidative damage and photo-damage repair enhancer (Hemanth Kumar et al., 2017). However, Antunes et al. (2014) reported hesperidin (50 mg/kg) treatment attenuated the 6-OHDA-in- duced reduction in GPx, SOD and CAT levels in mouse model of Parkinson’s disease. Also, it is reported hesperidin increased glutathione, SOD, CAT and decreased MDA and nitrite level (Roohbakhsh et al., 2014). Administra- tion of hesperidin (20, 40 and 80 mg/kg) re- versed the levels of serum hepatic CAT, SOD, GPx and glutathione S-transferase (GST) en- zyme levels (Pari et al., 2015) which is sim- ilar to our result. New findings revealed the antioxidant activity of hesperidin mediates by radical scavenging activity and ERK/Nrf2 signaling pathway as well (Elavarasan et al., 2012). Injection of the hesperidin (0.5 and 1 mg/kg) during the GD significantly decreased MDA levels on postpartum mice compared to control group. Hesperidin has protective effect against reactive oxygen species (ROS) production and oxidative stress. Hesperidin enhanced antioxidant enzymes CAT, SOD and GST level (Visnagri et al., 2014). The enzymatic antioxidants CAT, SOD, GPx and GST have crucial role on scavenging ROS. Hesperidin has protective effect against oxi- dative damage due to the ability of enhanced antioxidant activity. There is a correlation between depressive disorders and increased oxidative stress, neuro-inflammation and di- minished anti-oxidant defenses (Black et al., 2014). The positive effect of the antioxidant effects of antidepressants in the treatment of
major depressive disorder is well documented (Da Silva et al., 2014).
Hesperidin–therapy is safe, has a non-ac- cumulative nature with lowest adverse effect, even during the pregnancy period (Hajialyani et al., 2019). Hesperidin administered at dos- es up to 5% for 13 weeks had no mutagenic, toxic, and carcinogenic effects on mice (Garg et al., 2001). In the model of rat colon car- cinogenesis, hesperidin decreased intestinal tumor incidents via antioxidant defense with no toxicity to the liver and colon (Aranga- nathan and Nalini, 2009). Hesperidin is able to decrease streptozotocin–isoproterenol-in- duced myocardial toxicity (Agrawal et al., 2014). Although hesperidin is a safe phyto- chemical, possible interactions of this phy- tochemical should be considered (Hajialyani et al., 2019). In view of our findings, the ob- tained data indicate hesperidin has protective activity against postpartum depression. How- ever, further research is needed to clarify the precise molecular mechanisms involved in the antidepressant effects of the hesperidin.
The authors thank the Faculty of Vet- erinary Medicine, Science and Research Branch, Tehran, Iran for their cooperation. This research was conducted as a part of the DVM thesis of the first author.
Conflicts of interest
The authors declared that there are no conflicts of interest.
Agrawal, Y.O., Sharma, P.K., Shrivastava, B., Arya, D.S., Goyal, S.N. (2014) Hesperidin blunts strep- tozotocin–isoproternol induced myocardial toxic- ity in rats by altering of PPAR-gamma receptor. Chem Biol Interact, 19, 211–220. https://doi.org/
Alimohammadi, S., Hosseini, M.S., Behbood, L. (2019) Prenatal exposure to zinc oxide nanoparti- cles can induce depressive- like behaviors in mice offspring. Int J Peptide Res Ther, 25(1), 401–409. https://doi.org/ 10.1007/s10989-018-9686-9
Amin, B., Nakhsaz, A., Hosseinzadeh, H. (2015) Evaluation of the antidepressant-like effects of acute and sub-acute administration of crocin and crocetin in mice. Avicenna J Phytomed, 5 (5), 458-468. PMID:26468466
Antunes, M.S., Goes, A.T., Boeira, S.P., Prigol, M., Jesse, C.R. (2014) Protective effect of hes- peridin in a model of Parkinson's disease in- duced by 6-hydroxydopamine in aged mice. Nutrition,104,19–26. https://doi.org/ 10.1016/j. nut.2014.03.024 PMID: 25280422
Aranganathan, S., Nalini N. (2009) Efficacy of the potential chemopreventive agent, hesperetin (citrus flavanone), on 1,2-dimethylhydrazine induced colon carcinogenesis. Food Chem Tox- icol, 47, 2594–2600. https://doi.org/ 10.1016/j.
fct.2009.07.019 PMID: 19632289
Black, C.N., Bot, M., Scheffer, P.G., Cuijpers, P., Penninx, B.W. (2014) Is depression associated with increased oxidative stress? A systematic re- view and meta-analysis. Psychoneuroendocrinol- ogy, 51c,164-175. https://doi.org/ 10.1016/j.psyn- euen.2014.09.025 PMID: 25462890
Castagné, V., Moser, P., Roux, S., Porsolt, R.D. (2011) Rodent models of depression: forced swim and tail suspension behavioral despair tests in rats and mice. Curr Protoc Neurosci, https:// doi.org/10.1002/04711 42301 .ns081 0as55 PMID:21462162
Cryan, J.F., Mombereau, C., Vassout, A. (2005) The tail suspension test as a model for assessing an- tidepressant activity: review of pharmacological and genetic studies in mice. Neurosci Biobehav Rev, 29(4–5),571–625. https://doi.org/ 10.1016/j. neubiorev.2005.03.009 PMID: 15890404
Da Silva, A.I., Monteiro Galindo, L.C., Nascimento, L., Moura Freitas, C., Lagranha, C.J., Lopes de Souza, S. (2014) Fluoxetine treatment of rat ne- onates significantly reduces oxidative stress in the hippocampus and in behavioral indicators of anxiety later in postnatal life. Can J Physiol Phar- macol, 92,330-337. https://doi.org/ 10.1139/cjpp- 2013-0321 PMID: 24708216
Donato, F., de Gomes, M.G., Goes, A.T., Filho,
C.B., Del Fabbro, L., Antunes, M.S., et al. (2014) Hesperidin exerts antidepressant-like effects in acute and chronic treatments in mice: possi- ble role of l-arginine-NOcGMP pathway and BDNF levels. Brain Res Bull, 104, 19–26. https:// doi.org/ 10.1016/j.brainresbull.2014.03.004 PMID: 24709058
El-Marasy, S.A., Abdallah, H.M.I., El-Shenawy, S.M., El-Khatib, A.S., El-Shabrawy, O.A., Ken- awy, S.A. (2014) Anti-depressant effect of hes- peridin in diabetic rats. Can J Physiol Pharmacol, 92, 945–952. https://doi.org/ 10.1139/cjpp-2014-
0281 PMID: 25358020
Filho, C.B., Souza, L.C., de Gomes, M.C. et al. (2013) Kappa-opioid receptorsmediate the an- tidepressant-like activity of hesperidin in the mouse forced swimming test. Eur J Pharmacol, 698(1-3), 286–291. https://doi.org/ 10.1016/j.ej-
phar.2012.11.003 PMID: 23178563
Garg, A., Garg, S., Zaneveld, L., Singla, A. (2001) Chemistry and pharmacology of the citrus biofla- vonoid hesperidin. Phytother Res, 15, 655–669. https://doi.org/ 10.1002/ptr.1074 PMID: 11746857
Gu, X., Zhou, Y., Wu, X., Wang, F., Zhang, C.Y., Du,
C., Shen, L., Chen, X., Shi, J., Liu, C., Ke, K.
(2014) Antidepressant-like effects of auraptenol in mice. Sci Rep, 4,4433. https://doi.org/ 10.1038/ srep04433 PMID: 24658501
Hajialyani, M., Farzaei, M.H., Echeverría, J., Naba- vi, S.M., Uriarte, E., Sobarzo-Sánchez, E. (2019) Hesperidin as a neuroprotective agent: A review of animal and clinical evidence. Molecules, 24, 648. https://doi.org/10.3390/molecules24030648 PMID:30759833
Hemanth kumar, B., Dinesh kumar, B., Diwan,
P.V. (2017) Hesperidin, a citrus flavonoid, pro- tects against l-methionine-induced hyperhomo- cysteinemia by abrogation of oxidative stress, endothelial dysfunction and neurotoxicity in Wistar rats. Pharm Biol, 55, 146-155. https:// doi.org/ 10.1080/13880209.2016.1231695 PMID: 27677544
Khan, M.H.A., Parvez, S. (2015) Hesperidin ame- liorates heavy metal induced toxicity mediat- ed by oxidative stress in brain of Wistar rats. J Trace Elem Med Biol, 31, 53-60. https://doi.org/ 10.1016/j.jtemb.2015.03.002 PMID: 26004892
Khan, M.M., Raza, S.S., Javed, H., Ahmad, A., Khan, A., Islam, F., et al. (2012) Rutin protects dopaminergic neurons from oxidative stress in an animal model of Parkinson’s disease. Neurotox Res, 22,1–15. https://doi.org/ 10.1007/s12640- 011-9295-2 PMID: 22194158
Li, C. Schluesener, H. (2017) Health-promoting ef- fects of the citrus flavanone hesperidin. Crit Rev Food Sci Nutr, 57, 613-631. https://doi.org/ 10.1080/10408398.2014.906382 PMID: 25675136
Matias, I., Diniz, L.P., Buosi, A., Neves, G., Sti- pursky, J., Gomes, F.C.A. (2017) Flavonoid hesperidin induces synapse formation and im- proves memory performance through the astro- cytic TGF-β1. Front. Aging Neurosci, 9,184. https://doi.org/10.3389/fnagi.2017.00184 PMID: 28659786
Menze, E.T., Tadros, M.G., Abdel-Tawab, A.M., Khalifa, A.E. (2012) Potential neuroprotective effects of hesperidin on 3-nitropropionic ac- id-induced neurotoxicity in rats. Neurotoxicol- ogy, 33,1265–75. https://doi.org/ 10.1016/j.neu- ro.2012.07.007 PMID: 22850463
Ming, L.I., Shinn-Yi, C. (2016) Modeling postpar- tum depression in rats: theoretic and method- ological issues. Zool Res, 37(4), 229–236. https:// doi.org/ 10.13918/j.issn.2095-8137.2016.4.229 PMID: 27469254
O'Hara, M.W., McCabe, J.E. (2013) Postpartum de- pression: current status and future directions. Ann Rev Clin Psychol, 9 (1), 379- 407. https://doi. org/ 10.1146/annurev-clinpsy-050212-185612 PMID: 23394227
Pari, L., Karthikeyan, A., Karthika, P., Rathinam, A. (2015) Protective effects of hesperidin on oxida- tive stress,dyslipidaemia and histological changes in iron-inducedhepatic and renal toxicity in rats. Toxicol Rep, 2: 46–55. https://doi.org/10.1016/j.
toxrep.2014.11.003 PMID: 28962336
Perani, C.V., Slattery, D.A. (2014) Using animal mod- els to study post-partum psychiatric disorders. Br J Pharmacol, 171(20), 4539–4555. https://doi.
org/10.1111/bph.12640 PMID: 24527704
Roohbakhsh, A., Parhiz, H., Soltani, F., Rezaee, R., Iranshahi, M. (2014) Neuropharmacological properties and pharmacokinetics of the citrus fla- vonoids hesperidin and hesperetin — A mini-re- view. Life Sci, 113,1–6. https://doi.org/ 10.1016/j. lfs.2014.07.029 PMID: 25109791
Saravi, S.S.S., Arefidoust, A., Yaftian, R., Saravi, S.S.S., Dehpour, A.R. (2016) 17 alpha-ethinyl estradiol attenuates depressive-like behav- ior through GABA(A) receptor activation/ni- trergic pathway blockade in ovariectomized mice. Psychopharmacology, 233, 1467–1485. https://doi.org/10.1007/s00213-016-4242-9 PMID: 26883875
Souza, L.C., de Gomes, M.G., Goes, A.T., Del Fab- bro, L., Carlos Filho, B., Boeira, S.P., Jesse, C.R. (2013) Evidence for the involvement of the se- rotonergic 5-HT 1A receptors in the antidepres- sant-like effect caused by hesperidin in mice. Prog Neuropsychopharmacol, 40, 103–109. https://doi.org/10.1016/j.pnpbp.2012.09.003 PMID: 22996046
Steru, L., Chermat, R., Thierry, B., Simon, P. (1985) The tail suspension test: a new method for screen- ing antidepressants in mice. Psychopharmacol- ogy, 85(3),367–370. https://doi.org/ 10.1007/ bf00428203 PMID: 3923523
Visnagri, A., Kandhare, A.D., Chakravarty, S., Ghosh, P., Bodhankar, S.L. (2014) Hesperidin, a flavanogly- cone attenuates experimental diabetic neuropathy via modulation of cellular and biochemical marker to improve nerve functions. Pharm Biol, 52,814–28. https://doi.org/ 10.3109/13880209.2013.870584 PMID: 24559476
Walia, V., Gilhotra, N. (2016) Nitriergic influence in the compromised antidepressant effect of fluoxe- tine in stressed mice. J Appl Pharm Sci, 6 (10),092-
تعداد مشاهده مقاله: 695
تعداد دریافت فایل اصل مقاله: 332