Moringa Oleifera leaves have therapeutic functions such as antioxidant, anti-bacterial, antiviral, anti-cancer, anti-inflammatory, anti-allergic and anti-diabetic. The purpose of this study was to evaluate the protective effect of Moringa Oleifera on obesity induced oxidative stress and biochemical abnormalities in male rats. Forty-eight male albino rats were divided into three equal groups. Group I (control normal): rats fed normal diet. Group II (Obesity): rats received high fat diet (HFD).Group III (Obesity+ Moringa oleifera): rats received Moringa Oleifera (600 mg/kg.b.wt.) orally for two months after induction of obesity. The obtained results showed significant increase in levels of serum insulin, lipids profile (total cholesterol and triacylglycerols), liver L-MDA in addition to up regulation of Leptin and Nuclear factor kappa B (NF-κB) gene expression level in obese rats. However, liver catalase activity and GSH concentration were markedly decreased. Moringa Oleifera treatment to high fat dietinduced obesity in rats caused significant improvement of all previous parameters towards its normal ranges. These results suggested that, Moringa Oleifera treatment exerts a protective effect on obesity by reduction of oxidative stress markers, inflammation and hyperlipidemia in rats through free radical scavenging and anti-inflammatory activities as well as regenerating endogenous antioxidant defense system mechanisms.

Premature ovarian failure (POF) is a cessation of ovarian function in women less than 40 years old. The atrophy of the ovary leads to decreased follicle storage, which leads to irregular of the menstrual cycle, dysfunction of the ovary and causes infertility. The current study was conducted to investigate the effects of curcumin (CRC) and hesperidin (HSP) on POF in a female rat. POF was Caused by intraperitoneal (i. p.) injection of cyclophosphamide (200 mg/kg b. wt.) at the first day and then (8 mg/kg b. wt./day) for the next 14 days. The treatment with CRC (100 mg/kg b. wt./day, i. p) and / or HSP (80 mg/kg b. wt./day, i. p.) were started and continued for 14 days after two weeks for POF induction. Ninety female rats were classified into six groups. Group 1 (Control), Group 2 (POF-induced), Group 3 (POF+ CRC), Group 4 (POF+HSP), Group 5 (POF+CRC+HSP) and Group 6 (Normal+CRC+HSP). Serum follicle-stimulating hormone (FSH) and ovarian tissues malondialdehyde (MDA) concentrations significantly increased, while serum estradiol (E2) level, ovarian tissues reduced glutathione (GSH) and superoxide dismutase (SOD) markedly decreased in POF group as compared with the control group. However, the 3 rd , the 4 th and the 5 th treated groups had a significant increase in serum E2, ovarian tissues SOD activity and GSH level and marked decrease in FSH and MDA concentrations compared with the POF group. The histopathological changes in the three treated groups improved toward control group. Conclusively, Hesperidin superior to curcumin in the alleviation of oxidative stress and hormonal alterations in a rat model of cyclophosphamide-induced premature ovarian failure.

Proanthocyanidins, also known as condensed tannins, can prevent obesity induced oxidative stress damage in the liver. This study aimed to evaluate the protective effect of Proanthocyanidins on obesity induced oxidative stress and biochemical abnormalities in male rats. Forty-eight male albino rats were divided into three equal groups. Group I (control normal): rats received normal diet. Group II (Obesity): rats received high fat diet (HFD). Group III (Obesity+ Proanthocyanidins): rats received Proanthocyanidins (50 mg/kg.b.wt.) orally for two months after induction of obesity. The obtained results showed significant increase in serum insulin, lipids profile (total cholesterol and triacylglycerols) concentrations, liver L-MDA in addition to up regulation of leptin and Nuclear factor kappa B (NF-κB) gene expression level in liver tissues of obese rats. However, liver catalase activity and GSH concentration were markedly decreased. These results suggested that, Proanthocyanidins treatment exerts a protective effect on obesity by reduction of oxidative stress, inflammation and hyperlipidemia in rats through free radical scavenging and anti-inflammatory activities as well as regenerating endogenous antioxidant defense system mechanisms.

In the present study the gastroprotective effect and the molecular mechanisms of probiotics in a rat model of ethanol-induced gastric injury were evaluated. Thirty-five male rats were divided into five equal groups. Group 1: (Control normal group) rats received no drugs. Group 2: (Early ulcer non-protected group) rats received absolute ethanol (0.5ml/100g rat) orally on an empty stomach and sacrificed one hour later. Group 3: (Probiotics protected group) rats received probiotic (135 mg/kg body weight/day) orally for 21 days before ethanol administration then sacrificed one hour after ethanol administration. Group 4: (Late ulcer non-treated group) rats received absolute ethanol (0.5 ml/100g rat) orally on empty stomach and sacrificed after 21 days. Group5: (Late ulcer + Probiotics treated group) rats first administered with absolute ethanol (0.5 ml/100g rat) on empty stomach at the first day of experiment then after one hour, probiotic was administered (135 mg/kg body weight/day) for 21 days then sacrificed. The results showed a significant increase in L-Malondialdehyde (L-MDA) and decrease in reduced glutathione (GSH) concentration and Catalase (CAT) activity in stomach of gastric injuryinduced in rats as compared with control group. Conversely, a significant decrease in L-MDA and obvious increase in GSH concentration and CAT activity were observed after probiotics treatment when compared to gastric ulcerated rats. Likewise, a significant up-regulation of nuclear transcription factor kappa-B (NF-κB) gene expression level was observed in stomach of ulcerated rats. This expression was downregulated after probiotics administration. Meanwhile, a significant down-regulation of peroxisome proliferator-activated receptor gamma (PPARγ) and transforming growth factor β1 (TGF-β1) gene were detected in ethanolinduced rat gastric injury. This expression was upregulated after probiotics administration. Conclusively, probiotics improving gastric cell proliferation and protect gastric mucosa against injury-induced in rats via anti-inflammatory and anti-oxidative mechanisms.

Gastric ulcer is a common chronic disease in human digestive system. Massive alcohol drinking can lead to gastric ulcer. The gastroprotective effect and molecular mechanisms of Proanthocyanidin in a rat model of ethanol-induced gastric mucosal erosion were investigated. Thirty-five male rats were divided into five equal groups. Group 1 (Control normal): rats received no drugs. Group 2 (Early ulcer): rats received absolute ethanol (0.5 ml/100g) orally on empty stomach and sacrificed one hour later. Group 3 (Early ulcer + Proanthocyanidin protected): rats received proanthocyanidin orally at a dose of (300 mg/kg b. wt/day) for 3 weeks before ethanol administration then sacrificed after one hour. Group 4 (Late ulcer): rats received ethanol like group 2 and sacrificed after 21 days. Group 5 (Late ulcer + proanthocyanidin treated): rats first administered ethanol (0.5 ml/100g) and after one-hour proanthocyanidin was administered for 21 days. A significant increase in stomach L-MDA concentration with marked decrease in CAT activity and GSH concentration were observed in gastric erosion-induced rats. However, a significant depletion of gastric L-MDA level and marked increase in CAT activity and GSH concentration were observed after Proanthocyanidin treatment when compared to ulcerated rats. A significant up-regulation of gene expression level of BAX, NF-κB and IL-1β with downregulation of Bcl-2 gene were observed in stomach of gastric erosion-induced rats. However, a significant down regulation of BAX, NF-κB and IL-1β with up-regulation of Bcl-2 gene were observed after proanthocyanidin treatment. Conclusively, proanthocyanidin protects rat gastric mucosa against ethanol-induced gastric erosion via anti-inflammatory, anti-apoptotic and antioxidative mechanisms.