The effect of hydroethanolic extract of Matricaria chamomilla on the reproductive system of male rats exposed to formaldehyde.

Formaldehyde is a common agent in our surrounding environment and can adversely affect the male reproductive system. In this study, the effectiveness of Matricaria chamomilla (MC) extract as an antioxidant was investigated in rats treated with formaldehyde. Thirty-two male Wistar rats were randomly divided into six groups: F (10 mg/kg formaldehyde), M200 (200 mg/kg MC extract), M500 (500 mg/kg MC extract), FM200 (10 mg/kg formaldehyde and 200 mg/kg MC extract), FM500 (10 mg/kg formaldehyde and 500 mg/kg MC extract) and control group (0.9% normal saline). Formaldehyde and MC extract were administered daily for 30 consecutive days via intraperitoneal injection. Hormonal status, sperm parameters, testis tissue histology, germinal cells apoptosis and stereological analyses of testis tissue were investigated. Testosterone and LH levels were significantly increased in FM200, FM500, F200 and F500 groups compared to F group (p ≤ 0.05). Sperm count, motility and viability were significantly enhanced in FM200, FM500, F200 and F500 groups compared to F group (p ≤ 0.05). A decrease in the number of apoptotic germ cells in FM200, FM500, M200 and M500 groups (p ≤ 0.05) was evident. In particular, the MC extract in dose 500 mg/kg is seen to reduce the adverse effects of formaldehyde on the reproductive system of male rats.

Antioxidant and neuroprotective effects of lycopene and insulin in the hippocampus of streptozotocin-induced diabetic rats.

In the present study the antioxidant and neuroprotective effects of insulin and lycopene on passive avoidance memory, total antioxidant capacity (TAC), malondialdehyde activity (MDA) and prevention of apoptosis in the hippocampus streptozotocin-induced diabetic rats were examined. The rats were randomly divided to six experimental groups (n=8 per group): Non-diabetic (controls); diabetic; diabetic treated with lycopene; diabetic treated with insulin; diabetic treated with lycopene and insulin; and normal treated with lycopene. Intraperitoneal injection of single dose (60 mg/kg) streptozotocin (STZ) was used to induce the diabetes rat model. The shuttle box test was used for learning and memory assessment. Rats were then sacrificed and hippocampi tissue isolated from the two hemispheres to determine TAC and MDA. Apoptosis rate was also evaluated by terminal deoxynucleotidyl transferase dUTP nick-end labeling and acridine orange staining assays. The results indicated that lycopene and insulin, solely or in combination, prevented hippocampal neuronal cell death and improved learning and cognition by increasing TAC and decreasing MDA. Collectively, the findings presented herein suggest that insulin and lycopene co-treatment has neuroprotective effect, and ameliorates STZ-induced learning and memory impairment and apoptotic cell death in the hippocampal regions of diabetic rats.

Neuroprotective effect of lovastatin through down-regulation of pro-apoptotic Mst1 gene expression in rat model pilocarpine epilepsy.

OBJECTIVE: Statins as inhibitors of HMG-CoA reductase have been recently recognized as anti-inflammatory and neuroprotective drugs. In this paper, we studied anti-apoptotic and regulatory effects of lovastatin using Pilocarpine rat model through downregulation of Mst1 (Mammalian sterile 20-like kinase 1) as a novel pro-apoptotic gene. METHODS: The rats were divided into four groups: non-treated epileptic rats, lovastatin treated, and two vehicle groups. Racine scale was used for behavioral assessment and animals with a score of 4-5 were selected for the study. After 3 days, epileptic rats received intraperitoneal injections of lovastatin, followed by treating for 14 days. Next, they were sacrificed (28 post-first seizure) and prepared for histopathological analysis and Real-time RT-PCR. RESULTS: The results showed that lovastatin protects Pilocarpine-induced cell death via a regulatory effect on pro-apoptotic and anti-apoptotic gene expression. The real-time PCR results showed that in the epileptic lovastatin treated group, the expression level of Mst1 significantly decreased while Nrf2 and Bcl-2 genes increased. Furthermore, histological analysis of neurodegeneration in the brain sections showed that the number of hippocampal apoptotic cells significantly decreased in the treatment groups. The results showed that the numerical density of neurons per area was significantly higher in the treated than the untreated group. CONCLUSION: Overall, the results of this study showed that lovastatin attenuates hippocampal cell death in Pilocarpine-induced status epilepticus rat model through downregulation of the pro-apoptotic Mst1 gene. ABBREVIATIONS: Mst1: Mammalian sterile 20-like kinase 1; Nrf2: nuclear factor erythroid 2-related factor 2; Bcl-2: B-cell lymphoma 2; HMG-CoA: 3-hydroxy-3-methylglutaryl-coenzyme A; RT-PCR: reverse transcription-polymerase chain reaction; TLE: Temporal Lobe Epilepsy; SE: status epilepticus.

Risk factors of placental abruption.

BACKGROUND: Placental abruption is one of the most common causes of bleeding during pregnancy. Multiple factors are known to be associated with increase of risk of placental abruption such as alcohol, cocaine use and cigarette smoking. The objective of this study was to identify risk factors for placental abruption in an Iranian women population. MATERIALS AND METHODS: In a retrospective case - control study birth records included 78 cases with placental abruption and 780 randomly selected controls were investigated. Statistical analysis for comparing the studied risk factors between groups was performed using Pearson's Chi-square test along with presenting relevant odds ratio (OR). RESULTS: From 7301 deliveries included in the study, 78 (1%) was complicated placental abruption. Women aged 35 or more likely for experiencing (OR = 3.650, 95% confidence interval [CL] = 1.57-6.83) and those who had a previous cesarean section (OR = 2.65, 95% CL = 3.91- 33.41) were in higher risk for placental abruption ([50 cases] 64% vs. [28 cases] 36% P < 0.01). CONCLUSION: The results indicate that among the placental abruption is one of the most common causes of bleeding during the pregnancy and one of the major obstetrical emergency.

The relationship between retinol-binding protein 4 levels, insulin resistance, androgen hormones and polycystic ovary syndrome.

BACKGROUND: Retinol-binding protein 4 (RPB4), a 21-kDa peptide, is a recently identified adipokine that may contribute to the pathogenesis of polycystic ovary syndrome (PCOS). The aim of this study was to explore the association between serum RBP4 levels, androgen hormones and insulin resistance (IR) in women with PCOS. METHODS: In this case-control study, 75 PCOS patients and 53 age- and body mass index (BMI)-matched control subjects referred to the Zanjan Metabolic Disease Research Center were enrolled. Serum RBP4 was measured using an enzyme-linked immunosorbent assay. BMI, waist circumference (WC), fasting levels of glucose, lipid profiles and insulin were also measured. A homeostatic model assessment of insulin resistance (HOMA-IR) value was used to determine the level of insulin resistance. RESULTS: PCOS cases had significantly higher serum RBP4 and insulin levels than control subjects (44130 ± 12760 vs. 32980 ± 9560 µg/L, p < 0.001, and 11790 ± 11480 vs. 7890 ± 4300 µU/L, p < 0.05, respectively), in univariable analysis. RBP4 showed a positive correlation with serum testosterone (r = 0.62, p < 0.0001), dehydroepiandrosterone sulfate (r = 0.45, p < 0.0001) and the waist circumference (r = 0.37, p < 0.001) of PCOS patients but not with other measured clinical and biochemical variables. However, no correlation was observed between serum RBP4 levels and HOMA-IR in all studied subjects. A final logistic regression analysis demonstrated that testosterone and dehydroepiandrosterone sulfate are independently associated with PCOS. CONCLUSION: These findings indicate that RBP4 is not independently associated with PCOS. The elevation of RBP4 levels in PCOS women might be influenced by androgen hormones. Further prospective studies are needed to clarify molecular mechanisms.

Intraperitoneal aminoguanidine improves sciatic nerve ischemia-reperfusion injury in male sprague-dawley rats.

The present work was designed to investigate the potential protective effects of post-ischemic treatment with aminoguanidine (AG) on sciatic nerve ischemia/reperfusion (I/R) injury in rat. Seventy-two rats were divided into 12 groups (n = 6). We used ischemia model in these groups by occluding the right common iliac and femoral arteries for 3 h with a silk suture 6-0 using slipknot technique. Treatment groups (2, 4, 6, 8, 10, and 12) received 150 mg/kg AG intraperitoneally 24 h after induction of ischemia. After certain time intervals of reperfusion (2, 4, 7, 14, and 28 days), the function of the hind limb was assessed using behavioral scores based on gait, racing reflex, toe spread, pinch sensitivity, paw position, and grasp. After euthanasia, sciatic nerves were removed at the end of reperfusion times and sections were cut at 5 µm, then were stained for light microscopy studies and graded for ischemic fiber degeneration (IFD), edema, and apoptosis. Maximal behavioral deficit occurred at 7 days of reperfusion. The comparison of behavioral score pertaining to the control and AG groups revealed significant differences and showed also a better time course in recovery (P < 0.05). Other than 3 and 4 groups, the amount of edema in AG treatment groups showed significant differences compared with control groups (P < 0.05). IFD was also significantly decreased in the AG treatment groups than controls. Most importantly, I/R-induced apoptosis were improved significantly on the 4th, 7(th), and 14th days of reperfusion in AG-treated groups compared to controls. In conclusion, our findings suggest that post-ischemic administration of AG exhibits protective effect against sciatic nerve I/R injury.

The effects of simvastatin on ischemia-reperfusion injury of sciatic nerve in adult rats.

Severe ischemia to nerve results in fiber degeneration and reperfusion results in oxidative injury to endothelial cells and augments fiber degeneration. Statins, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, the most widely used lipid-lowering drugs, have been demonstrated to play a neuroprotective role. So we evaluated the effectiveness of simvastatin in protecting sciatic nerve from ischemia-reperfusion injury using the model of experimental nerve ischemia. Sixty adult male Sprague-Dawley rats weighing 250-300 g were used. They were divided into ten groups (N=6 per group). We used ischemia model in these groups by occluding the femoral artery and vein with a silk suture 6-0 using slipknot technique. All ischemia groups were rendered in ischemic for 3 h reperfused for various times of zero (0 h), 3 h (3 hour reperfusion), 7 days (7 day reperfusion), 14 days (14 day reperfusion). Half of the groups had experimental simvastatin (1 mg/kg) i.v. injection treatment via tail vein 1 h before ischemia. The other half experienced only ischemia-reperfusion as control groups. After euthanasia, histological samples were taken from distal part of the sciatic nerve. Sections were cut at 5 microm and then were stained with H and E and modified trichrome. We used H and E stain for edema and trichrome gomori for ischemic fiber degeneration. Samples were observed to assess their fiber degeneration and edema changes. By observation the level of fiber degeneration and endoneurial edema were also decreased in these recent groups (in both ischemia and reperfusion duration). In conclusion, pre-ischemic administration of simvastatin exhibits neuroprotective properties in ischemia-reperfusion nerve injury.

The effects of simvastatin on functional recovery of rat reperfused sciatic nerve.

This study evaluated the effectiveness of simvastatin in protecting sciatic nerve from ischemia-reperfusion (I/R) injury using the model of experimental nerve ischemia. Sixty adult male Sprague-Dawley rats weighing 250-300 g were used. They were divided into ten groups (N = 6 per group). We used ischemia model in these groups. All ischemia groups were rendered ischemic for 3 h. Then followed by reperfusion durations of zero time (0 hR), 3 h (3 hR), 7 days (7 dR), 14 days (14 dR). The treatment group received intravenous simvastatin (1 mg kg(-1)) 1 h before ischemia, while the control group received an equal volume of intravenous vehicle at the same time schedule and route. Behavioral data were obtained immediately before euthanasia. The score was based on coordination, racing reflex, toe spread and reaction to pinch. In simvastatin treated I/R rats we had increase in functional recovery. In conclusion, pre-ischemic administration of simvastatin exhibits neuroprotective properties in I/R nerve injury.