Effect of apple vinegar on folliculogenesis and ovarian kisspeptin in a high-fat diet-induced nonalcoholic fatty liver disease in rat.

BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) adversely affects reproduction. We aimed to study the effect of a high-fat diet (HFD), supplemented with apple vinegar, on folliculogenesis in a rat model of NAFLD. METHODS: Female rats were randomly divided into four groups (N = 28): Standard diet (SD), SD + vinegar, HFD, and HFD + vinegar groups. At the end of the study, biochemical tests were assessed in serum. HOMA-IR (Homeostatic model assessment-Insulin resistance) was calculated. Sex hormones were determined using an ELISA kit; ovary follicle counts were studied using histological methods. The proliferation index of granulosa cells was determined using immunohistochemistry. Kisspeptin expression in the ovary was detected using RT-PCR. RESULTS: The HFD induced steatohepatitis and NAFLD. The ovaries in the rat model of NAFLD were atrophied. The ovaries had less count of developing follicles and corpus luteum, and more degenerated and cystic follicles in comparison with the SD group. Vinegar + HFD consumption decreased ALT, compared to the HFD group (P = 0.004). Steatohepatitis was reduced in the Vinegar + HFD group (P = 0.001). Vinegar + HFD considerably reduced HOMA-IR (p = 0.01). The HFD + vinegar diet could increase estradiol (P = 0.001), without significantly affecting progesterone or testosterone. In addition, an increase of primordial follicles as an ovarian reserve and also primary follicles were determined in the HFD + vinegar group. There were no statistical differences in the granulosa cell proliferation index in various follicle types between groups. HFD + vinegar significantly enhanced ovarian kisspeptin expression (p = 0.04). CONCLUSIONS: The vinegar diet in a rat model of NAFLD raises estradiol, primordial, and small primary follicles, and increases ovarian kisspeptin expression indirectly. Insulin resistance and obesity were improved by apple vinegar, and anti-glycemic and anti-lipidemic effects were also determined. The supplementation of apple vinegar in NAFLD might be useful for ovary. However, it requires further investigation.

Ginseng alleviates folliculogenesis disorders via induction of cell proliferation and downregulation of apoptotic markers in nicotine-treated mice.

BACKGROUND: Ginseng is a powerful phytoestrogen with high antioxidant properties. OBJECTIVE: This study aimed to evaluate the effect of Panax Ginseng (PG) on folliculogenesis, proliferation, and apoptosis in the ovary impaired by nicotine. METHODS: Forty adult mice were divided into five groups. Control, sham, and nicotine groups, and co-treated groups of nicotine and ginseng in doses of 0.5 and 1 g/kg. Folliculogenesis was assessed via histopathology and serum evaluation of estradiol, progesterone, follicle-stimulating hormone (FSH), and luteinizing hormone (LH) by ELISA. Lipid peroxidation and antioxidant enzyme activities both in homogenate tissue and serum were assayed by colorimetric analysis. Apoptotic markers of cytochrome c (Cyt c), Bax, and Bcl-2 were evaluated by RT-PCR. Proliferative index was studied by the Ki-67 immunostaining procedure. RESULTS: In comparison to the control or sham groups, nicotine significantly reduced the levels of FSH, LH, and estradiol hormones. An insignificant reduction was observed in the progesterone hormone. Nicotine reduced all healthy follicle numbers, except primordial (P = 0.001). Malondialdehyde (MDA) was increased in tissue and serum in the nicotine group (P = 0.01). Serum catalase (CAT) and enzymatic activity of superoxide dismutase (SOD) both were reduced in tissue and the serum, in the nicotine group. Nicotine induced a reduction in the proliferative indexes of granulosa and theca cells in pre-antral and antral follicles (P = 0.001). However, its effect on the proliferative index of stroma cells was not significant. Apoptotic markers were elevated in the nicotine group (P = 0.001). Co-treatment with ginseng elevated all sex hormones, increased healthy follicles, and reduced tissue or serum lipid peroxidation, compared with the nicotine group (p < 0.05). Co-Treatment with ginseng also reduced the expression of apoptotic markers and increased the proliferative indexes in granulosa and theca cells in pre-antral and antral follicles and also in stroma cells, in comparison to the nicotine group (P = 0.001). All above-mentioned alterations following treatment with ginseng were remarkable, especially in the dose of 1 g/kg. CONCLUSION: This study showed ginseng protects folliculogenesis via alteration of hypothalamic- pituitary-gonadal (HPG) axis, induction of proliferation in ovarian somatic cells, reduction of lipid peroxidation, and downregulation of apoptotic markers in the mouse ovary, treated with nicotine.

The amelioration of nicotine-induced reproductive impairment in male mouse by Sambucus ebulus L. fruit extract.

Nicotine as a toxic agent in cigarette smoke impairs the reproductive system. Sambucus ebulus extract (SEE) is shown to have some beneficial effects such as antioxidant properties. The aim of this study was to evaluate the effects of SEE on the hormones of the pituitary-gonadal axis, lipid peroxidation index, antioxidant enzymes, spermatogenesis, and epididymal sperm parameters in male mice treated with nicotine. Adult male mice were divided into five groups; A: normal saline, B: 1 mg/kg nicotine, C: 1 mg/kg nicotine and 10 mg/kg SEE, D: 1 mg/kg nicotine and 50 mg/kg SEE, D: 1 mg/kg nicotine and 100 mg/kg SEE. Treatments lasted for 35 days. The spermicidal activity of SEE was tested in vitro. Sperm count, motility and morphology were assessed for fertility. Serum testosterone, prolactin and luteinizing hormone (LH) were measured, using ELISA. Serum malondialdehyde (MDA), catalase (CAT), and superoxide dismutase (SOD) activity were measured, using colorimetric assays. Spermatogenesis was evaluated by Johnsen's score and morphometry in histological slides. SEE at different doses did not have any spermicidal activity. Sperm parameters were reduced in the nicotine-treated group, compared with controls (P<0.01). Nicotine reduced testosterone and LH levels (P<0.01) and increased prolactin (P<0.01). A hike in MDA and a reduction in SOD activity without change on CAT, were observed in the nicotine group. Nicotine caused hypospermatogenesis. SEE improved most of the above-mentioned parameters, especially in the doses of 50 and 100 mg/kg. Beneficial effects of SEE in the doses of 50 and 100 mg/kg on male reproduction impairment, induced by nicotine might be partly attributed to the reduction of oxidative stress and changes in the hormones of the pituitary-gonadal axis.

The effects of radiofrequency on the bacteriological and histological characteristics of tonsils in patients with chronic and persistent tonsillitis.

OBJECTIVES: Tonsillotomy with radiofrequency (RF) is one of the newest treatments for chronic tonsillitis, but the mechanism of RF effects and complications are still pending. The aim of this study was to evaluate the effects of RF on the histological and bacteriological characteristics of the tonsils (Case-control study). MATERIALS AND METHODS: In fifty-two patients with chronic tonsillitis in 2017-2018, immediately after tonsillectomy, the tonsils were divided into 2sections; one sample treated with RF, and the other one considered as control, without intervention. All tonsil samples sent for histological and bacteriological study: morphometric assays made by Digitizer software, and type of bacterial colonies identified by microbiological and biochemical tests. Willcoxon and McNemar tests were used for statistical analysis and level of significance was p ≤ .05. RESULTS: Tonsil mucosal thickness (2202.98 ± 323.09 vs. 2463.94 ± 357.61 µm) and size of the tonsil nodule (28,000.42 ± 9608.75 vs. 36,692.81 ± 7040.74 µm2) were significantly lower in the RF+ group than other group (p = .001 and p = .01, respectively). There was no significant differences in thickness of the tonsil epithelium (p = .075), number of lymphoid nodules (p = .860), and the number of reticular tonsil epithelium (p = .813) between the two groups. Bacterial growth in RF- and RF+ groups had no statistically significant difference (p = .06), however, the average colony count of S. aureus in RF+ tonsils were significantly lower, and total number of bacterial colonies were significantly lower in RF+ group(1405 ± 156 vs. 2471 ± 156), (p = .001). CONCLUSION: RF surgery has significant effects on size of the nodules, thickness of the mucous layer and bacteriological characteristics of tonsil tissue. Especially S. aureus seems to be more sensitive to RF effects.

Cinnamaldehyde Enhanced Functional Recovery after Sciatic Nerve Crush Injury in Rats.

Peripheral nerve injury is a common clinical issue induced by trauma, tumor, and damage caused by treatment. Such factors create chemical and inflammatory alterations at the injury site, which increase nerve deterioration. Thus, minimizing these modifications can lead to nerve protection after injury. The present study sought to evaluate the possible improvement in nerve regeneration and enhancement of functional outcomes by cinnamaldehyde (Cin) administration following sciatic nerve crush in a rat model. Rats (n = 48) were distributed into 6 groups, including sham, injury, DMSO (vehicle group), and Cin groups (10, 30, and 90 mg/kg/day). Using small hemostatic forceps, crush injury was induced in the left sciatic nerve. Thereafter, Cin was administered for 28 successive days. Weekly records were taken for sciatic functional index (SFI) measurements. Further assessments including electrophysiological and histomorphometric evaluations, gastrocnemius muscle wet weight measurements, and estimation of the serum total oxidant status were performed. According to the results, Cin could accelerate sciatic nerve recovery after crush injury, and the dose of 30 mg/kg/day of Cin had better impacts on SFI recovery, muscle mass ratio, and myelin content. The current research demonstrated that Cin positively affects peripheral nerve restoration. Therefore, Cin therapy could be considered as a potential treatment method for peripheral nerve regeneration and its functional recovery. However, more investigations are required to further validate the study results and evaluate the optimal dose of Cin.

Supplementation of various zinc sources modify sexual development and testicular IGF family gene expression in pre-pubertal male Japanese quail.

Zinc plays an important role in the regulation of insulin-like growth factor-I (IGF-I). IGF system, in turn, has a key role in the development and functions of the reproductive organs. This research was performed to investigate the effects of different sources of zinc on IGF-I gene expression and testicular development in pre-pubertal male Japanese quail. A total of 512 unsexed day-old Japanese quail chicks were randomly divided into 16 groups (4 dietary treatments × 4 replicates) and kept for 35 days. The control group diet was not supplemented with zinc whereas the diets of three groups were supplemented with 25 mg kg-1 zinc oxide (ZnO), zinc oxide nanoparticle (ZnON), and zinc-methionine (Zn-Met). On days 28 and 35, one birds from each subgroup were weighed, bled, and euthanized to evaluate gonado-somatic index (GSI), testicular histology, serum testosterone concentration, cloacal gland index (CGI), and the testicular IGF family gene expression. The results showed that GSI was higher in ZnON (2.307) than control (1.619) on day 35 (P < .05). Germinal epithelium thickness was higher in ZnON (78.88 µm) and Zn-Met (79.73 µm) than control (67.73 µm) on day 35 (P < .05). On day 35, the testosterone concentration was lowest in the control (5.830 ng/ml, P < .05). The CGI of 35-day-old birds was higher in Zn-Met (411.28) than the control (307.59, P < .05). IGF-IR mRNA expression was highest in Zn-Met group on day 28. Therefore, supplementation of diet with Zn-methionine is superior to other sources of zinc for diet supplementation in immature Japanese quail.

Melatonin ameliorates testicular damages induced by nicotine in mice.

OBJECTIVES: Nicotine as a toxic substance leads to impairment of the reproductive system function. The aim of this study was to evaluate effects of melatonin on testicular alterations, sperm nuclear integrity, and epididymal sperm parameters in mice treated with nicotine. MATERIALS AND METHODS: Male mice were divided into four groups. Group A received the vehicle, group B received nicotine 0.1 mg/100 g BW, group C received melatonin 10 mg/kg, group D received nicotine plus melatonin. Evaluations were made by histology and Johnson's score for study of spermatogenesis, immunostaining for study of male germ cells apoptosis, sperm chromatin dispersion (SCD) test for assaying sperm chromatin integrity, enzyme-linked immunosorbent assay (ELISA) for assessment of serum levels of testosterone and luteinizing hormone (LH), and sperm parameters including morphology, motility, and count. RESULTS: Nicotine caused a significant decrease in spermatogenesis quantity and Johnson's score, sperm parameters, and sex hormones. Melatonin in group D, increased sperm chromatin integrity, improved spermatogenesis, Johnson's score, and sperm parameters (P<.01) and reduced apoptosis (P <0.01) in comparison with the nicotine group. Melatonin significantly increased testosterone and halo sperms. However, its effect on the LH level was insignificant. The serum testosterone and LH levels were negatively correlated with the DNA fragmentation index (DFI) (r= -0.86, P<0.001) and (r= -0.78, P<0.001), respectively. CONCLUSION: this study showed administration of melatonin in nicotine-treated mice increases both quality and quantity of spermatogenesis and integrity of sperm's chromatin through reducing apoptosis and modifying the testosterone level.

Beneficial effect of apple vinegar on reproductive parameters in male rat model of nonalcoholic fatty liver disease.

Nonalcoholic fatty liver disease (NAFLD) is associated with low testosterone levels in serum. The aim of this study was to evaluate the effect of apple vinegar on fertility indices in a rat model of NAFLD. To study this effect, 32 adult male rats were divided into four groups: A-normal diet, B-high-fat diet (HFD), C-apple vinegar and D-HFD plus apple vinegar. At the end of the week 22, the Lee index, serum lipid profiles, liver enzymes, glucose and total antioxidant levels (TAC) in serum were determined. In addition, liver and testis tissue homogenate, histopathology, serum testosterone and sperm parameters were measured and HOMA-IR calculated. Significant reduction in Lee index, serum triglyceride, cholesterol, liver enzymes and glucose levels was observed in vinegar treated group compared with HFD group. Vinegar lowered insulin resistance compared with HFD (p < 0.01). Steatosis in hepatocytes reduced from 56% in HFD group to 20% in group D (p < 0.05). Vinegar caused a significant increase in serum testosterone, improvement in sperm parameters and a reduced germ cell apoptosis (p < 0.05). There was an insignificant increase in TAC levels in the serum and homogenate tissue of liver and testis compared with HFD. This study reports apple vinegar has beneficial effects on male rat fertility indices in an in vivo model of NAFLD.

Comparative effects of zinc oxide, zinc oxide nanoparticle and zinc-methionine on hatchability and reproductive variables in male Japanese quail.

The objective was to examine the effect of different dietary zinc sources on reproduction of male Japanese quail. A total of 512 quail chicks (day-old) were divided into four groups with four replications for a period of 42 days. After this period, excess chicks were removed to attain the ratio of one male to three females and 16 quail in each subgroup. At 52 to 60 d of age, the eggs were collected and incubated. The basal diet (control) contained no zinc and the other three experimental diets were supplemented with 25 and 50 mg/kg zinc from zinc oxide (ZnO), zinc oxide nanoparticles (ZnONP) and zinc-methionine (Zn-Met) for 1 to 35 and 36 to 60 days, respectively. On day 42, two males from each replicate were euthanized. Males from the ZnO and Zn-Met treatments had an increase (P < 0.05) in seminiferous tubule diameters (STD) and germinal epithelium thickness (GET) compared with the control and ZnONP treatments. Cloacal gland index (CGI) was greatest (P < 0.05) for the Zn-Met compared with the other groups. Testosterone concentration was greater (P < 0.05) in the ZnO and Zn-Met compared with the other groups. Addition of Zn-Met to the diet enhanced (P < 0.05) fertility, hatchability and hatched chick weight compared with the other groups. Early and late embryonic death was greater (P < 0.05) in the control and ZnONP groups, respectively, compared with the other groups. This study indicated that supplementing diets with the Zn-Met source improves male Japanese quail reproductive performance and hatchability traits while zinc oxide nanoparticles have detrimental effects on male Japanese quail reproduction and reduces hatchability.

Administration of melatonin protects against acetylsalicylic acid-induced impairment of male reproductive function in mice.

OBJECTIVES: Melatonin, an important hormone secreted by the epiphysis, is a powerful anti-oxidant with a high potential to neutralize medical toxins. The goal of this study was to demonstrate the beneficial effect of melatonin on epididymal sperm and reproductive parameters in mice treated with acetylsalicylic acid (ASA). MATERIALS AND METHODS: Male adult mice were divided into four treatment groups: control, ASA, melatonin, and ASA+melatonin. Mice were administered ASA (50 mg/kg, orally) and/or melatonin (10 mg/kg, intraperitoneally), or vehicle control, for 14 days. Sperm count, sperm motility, and sperm morphology were evaluated to assess fertility. A colorimetric assay was used to measure serum total antioxidant capacity (TAC). A sperm chromatin dispersion (SCD) test was used to assess sperm chromatin integrity. Sex hormone levels were measured by ELISA. RESULTS: Compared to the control group, ASA treatment resulted in a significant decrease in sperm parameters (P<0.05), as well as a decrease in the integrity of sperm chromatin (P<0.01). ASA treatment also reduced serum testosterone and TAC levels (P<0.05). Co-administration of melatonin with ASA significantly improved epididymal sperm parameters and increased serum testosterone and TAC levels compared to the ASA-treated group. LH level was not different in the combined treatment group compared to control or ASA treatment. CONCLUSION: Short-term administration of ASA (50 mg/kg) has adverse effects on male reproductive function in mice. Co-administration of melatonin protects against ASA-induced impairment of male reproductive function by preventing the reduction in serum TAC and testosterone levels seen with ASA treatment alone.

Evaluation of Hepatoprotective Effect of Acantholimon Gilliati Eerial Part Methanolic Extract.

The aerial parts of Acantholimon gilliati was extracted by n-hexane, dichloromethane and methanol. Methanolic extract tested for hepatoprotective effects on formaldehyde liver injury in mice. The maximum effect that the methanolic extract showed protective effect on this experiment against formaldehyde observed in 5 and 10 mg. Also other concentrations of this extract showed positive effect compared to toxicant on morphology and biochemical factors of the liver. Results showed that the methanolic extract of the A. gilliati has a protective include functional and enzymatic stablingeffect on liver.

Ovarian and uterine alterations following forced swimming: An immunohistochemical study.

BACKGROUND: Physical exercise is known to be a stressor stimulus that leads to reproductive disruption. OBJECTIVE: The aim of this study was to evaluate the effect of forced swimming on the uterus and ovaries in mice. MATERIALS AND METHODS: Adult mice (N=24) were divided into the following three groups: A, control; B, swimming in water (10oC); and C, swimming in water (23oC). Swimmers swam for 5 min daily for 5 consecutive days/ wk during 2 wks. An enzyme linked immunosorbent assay was used to determine serum estradiol, follicle stimulating hormone (FSH) and testosterone levels. Immunohistochemistry was performed to study apoptotic cells or estrogen receptor (ER) expression in uterine epithelial cells and ovaries. ANOVA was used for statistical analysis. RESULTS: Swimming in both groups reduced the serum FSH and estradiol levels (p<0.01) without having a significant effect on the serum testosterone level or percentage of apoptosis in ovarian and uterine tissues (p<0.01) compared with controls. A significant reduction in the number of ERs in the uterus and ovaries, and secondary and graafian follicles were observed in groups B and C compared with controls (p<0.01); however the number of primordial and primary follicles were not significantly changed in the ovaries. CONCLUSION: Forced swimming of 2 wks duration reduces the serum levels of FSH and estradiol without having effects on apoptosis in the ovaries or uteri of mice. Over a long period of time, forced swimming may have an adverse effect on fertility.

Apoptotic and proliferative activity of mouse gastric mucosa following oral administration of fumonisin B1.

OBJECTIVES: Fumonisins are a group of toxic and carcinogenic mycotoxins, which contaminate the grains and their products. The aim of this study was to examine the apoptotic and proliferative activity of mouse gastric mucosa following administration of fumonisin B1 (FB1). MATERIALS AND METHODS: Twenty-nine female mice divided into treatment (n=15) and control (n=14) groups. The treatment group received FB1 (150 mg/kg diet) for 16 weeks. The gastric atrophy was allocated using grading criteria modeled on the updated Sydney System. Immunohistochemistry studies were performed for evaluation of apoptosis and proliferative activity in gastric mucosa. RESULTS: Mild to moderate gastric atrophy were observed in microscopic findings of the gastric mucosa in treated animals (P<0.05). Number of parietal cells significantly decreased in the treatment group in comparison with the control (P<0.05). Treatment with FB1 for 16 weeks significantly reduced both gastric mucosa height and mitotic index in the gastric glands (P<0.05). TUNEL- and Bax-labeled positive cell numbers significantly increased in the FB1-treated group compared to the control (P<0.05). In addition, proliferative activity of gastric glands in the treated group was significantly lower than the control (P<0.05). CONCLUSION: Oral administration of FB1 caused atrophy in gastric mucosa both via increasing of apoptosis and suppressing the mitotic activity of these cells.

Melatonin protects uterus and oviduct exposed to nicotine in mice.

Smoking is associated with higher infertility risk. The aim of this study was to evaluate protective effects of melatonin on the uterus and oviduct in mice exposed to nicotine. Adult female mice (n=32) were divided into four groups. Group A: control animals received normal saline, Group B: injected with nicotine 40µg/kg, Group C: injected with melatonin 10 µg, Group D: injected with nicotine 40µg/kg and melatonin 10 µg. All animals were treated over 15 days intraperitoneally. On the 16th day, animals in the estrus phase were dissected and their uterus and oviducts were removed. Immunohistochemistry was recruited for studying apoptosis and for detection of estrogen receptor (ER) alpha in luminal epithelium of the uterus and oviduct. Enzyme-linked immunosorbent assay was used for serum estradiol level determination. Nicotine in group B decreased estradiol level and ERalpha numbers both in the uterus and oviduct (p<0.05). Co-administration of melatonin-nicotine in Group D ameliorated the histology of the uterus and oviduct, increased ERalpha numbers and reduced apoptosis in the uterus and oviduct compared with the nicotine Group B (p<0.05). This study indicates that nicotine impairs the histology of the uterus and oviduct and co-administration of melatonin-nicotine ameliorates these findings, partly through alteration in ERalpha numbers and reduction of apoptosis.

Oxytocin protects cardiomyocytes from apoptosis induced by ischemia-reperfusion in rat heart: role of mitochondrial ATP-dependent potassium channel and permeability transition pore.

The current study examines the protective effect of oxytocin (OT) on cardiomyocyte apoptosis modulated by mitochondrial ATP-dependent potassium (mitoKATP) channel and permeability transition pore (mPTP) in the preconditioned myocardium of anesthetized rats. Eighty rats were equally divided into eight groups. The hearts of all animals except for the sham group were subjected to 25 min ischemia and 120 min reperfusion. Oxytocin, 5-hydroxydeconoate (5-HD), a specific inhibitor of the mitoKATP channel, and atractyloside (ATRC), an mPTP opener, were used prior to ischemia. Hemodynamic parameters were recorded throughout the experiment. Evaluations were made by infarct size, plasma lactate dehydrogenase level (LDH), transmission electron microscopy (TEM) and immunohistochemistry studies. OT prevented mean arterial pressure drop during early phase of ischemia and reperfusion. Treatment with OT before IR induction normalizes cardiomyocytes both in light microscopy and TEM observations. In addition, OT significantly reduced TUNEL- and increased Bcl-2-labeled positive cell number relative to IR (p<0.05). However, 5HD or ATRC inhibited the protective effects of OT on cardiomyocytes damaged by IR (p<0.05). Ultrastructural changes including extensive myofibril loss, sarcolemmal disruption and mitochondrial swelling due to amorphous dens bodies indicate necrosis induction in 5HD and ATRC as well as in IR groups. Restoration of immunohistochemistry parameters and protection against IR-induced ultrastructural changes confirm OT cardioprotective effects via mitoKATP channel and mPTP modulation in apoptosis induced by ischemia-reperfusion.

The Protective Effects of Exogenous Melatonin on Nicotine-induced Changes in Mouse Ovarian Follicles.

BACKGROUND: Nicotine exposure causes impaired fertility and ovarian dysfunction. The aim of this study was to investigate the possible protective role of melatonin, which is known as an antioxidant agent on altered ovarian functions upon nicotine exposure. METHODS: A total of 32 female adult NMRI mice were divided randomly into four groups (n = 8). The control group received vehicle, while group 2 received nicotine (40 µg/kg) for 15 days and group 3 melatonin (10 mg/kg) for 5 days. Group 4 received both nicotine (40 µg/kg) and melatonin (10 mg/kg) for the same periods. All animals were treated intraperitoneally. After autopsy on the 16th day, histopathological and morphometrical examinations were performed and serum estradiol concentrations were measured. The data were analyzed using ANOVA and Tukey post hoc test. A value of p < 0.05 was considered significant. RESULTS: Nicotine significantly reduced the number of pre-antral and antral follicles, as well as estradiol concentration compared to the control group (p < 0.05). However, the decrease in the number of primordial follicles was not significant in the nicotine treated group. A significant increase in the atretic follicles were observed in group 2 compared to the control group (p < 0.05). Moreover, melatonin caused a marked normalization in the number of ovarian follicles and estradiol levels in group 4 compared to group 2. CONCLUSION: The results from this study suggest that melatonin may have a protective effect against nicotine-induced ovarian changes on the number of different stages of follicle growth.

Role of endogenous oxytocin in cardiac ischemic preconditioning.

BACKGROUND: The aim of the present study is to assess the role of endogenous oxytocin (OT) in cardioprotective effects of ischemic preconditioning (IPC) in anesthetized rat. MATERIALS AND METHODS: Animals were divided into five groups: 1) ischemia-reperfusion (IR); (n=6), hearts were subjected to 25 min regional ischemia and 60 min reperfusion, 2) OT; (n=6), oxytocin was administered (0.03 µg/kg i.p) 10 min prior to ischemia, 3) IPC; (n=7), IPC was induced via a 5 min regional ischemia followed by 5 min of reperfusion before IR, 4) IPC+ATO (Atosiban); (n=6), atosiban (1.5 µg/kg i.p) was used as OT receptor selective antagonist in the beginning of IPC and 5) IR+ATO; (n=6), atosiban was injected 10 min prior to ischemia-reperfusion. RESULTS: In our experiment, Infarct size was decreased significantly in OT and IPC groups compared to IR (23 ± 1.5% and 19 ± 0.6% vs. 45 ± 2.9% in IR group, P<0.05). Administration of atosiban in IPC+ATO group increased infarct size to 39 ± 0.9% in comparison with OT and IPC groups (P<0.05). The use of OT and IPC prior to ischemia significantly declined ventricular arrhythmias severity in compared to IR group (1.2 ± 0.4 and 1 ± 0.5 respectively, vs. 4 ± 0.4 in IR group, P<0.05). Blockade of OT receptor by atosiban abolished the cardiopreconditioning effects of IPC. CONCLUSION: This study shows that, in part, the cardioprotective effects of IPC can be induced by endogenous OT.

Oxytocin protects rat heart against ischemia-reperfusion injury via pathway involving mitochondrial ATP-dependent potassium channel.

Cardiac preconditioning represents the most potent and consistently reproducible method of rescuing heart tissue from undergoing irreversible ischemic damage. One of the major goals of the current cardiovascular research is to identify a reliable cardioprotective intervention that can salvage ischemic myocardium. The aim of the present study is to evaluate the oxytocin (OT)-induced cardioprotection and the signaling pathway involved with mitochondrial ATP-dependent potassium (mitoKATP) channel in the anesthetized rat heart. Animals were divided into six groups (n=6): (1) IR; hearts were subjected to 25 min ischemia and 120 min reperfusion, (2) OT; oxytocin was administered (0.03 microg/kg i.p.) 25 min prior to ischemia, (3) ATO+OT; atosiban (ATO) was used as an OT-selective receptor antagonist (1.5 microg/kg i.p.) 10 min prior to OT administration, (4) ATO; atosiban was used 35 min prior to ischemia, (5) 5HD+OT; 5-hydroxydecanoic acid (5HD) was used as a specific inhibitor of mitoKATP channel (10mg/kg i.v.) 10 min prior to OT administration, (6) 5HD; 5HD was used 35min prior to ischemia. Then infarct size, ventricular arrhythmia and creatine kinase-MB isoenzyme (CK-MB) plasma level were measured. Hemodynamic parameters were recorded throughout the experiment. OT administration significantly decreased infarct size, CK-MB plasma level, severity and incidence of ventricular arrhythmia as compared to IR group. Administration of atosiban and 5HD abolished the cardiopreconditioning effect of OT. This study demonstrates that cardioprotective effects of OT are mediated through opening the mitoKATP channels.