Objective: Atypical antipsychotics represented a major advance in the treatment of schizophrenia and minimizing the extrapyramidal side effects. However, the use of atypical antipsychotics have been linked to weight gain, hyperglycemia, metabolic syndrome and risk of liver affection. Previous studies proposed that vitamin D deficiency may contribute to the development of insulin resistance, metabolic syndrome and more recently fatty liver. The goal of this study wasto investigate the role of vitamin D in protection against the metabolic and hepatic side effects of olanzapine. Methods: Eighteen female albino rats received treatment by gavage for 5 weeks and divided into; C group: received (0.5ml/day) of normal saline and olive oil (0.2ml) twice weekly, (O) group: received olanzapine (2mg/ kg/day) and olive oil (0.2ml) twice weekly, and (O+D) group: received olanzapine (2mg/kg/day) and vitamin D3 (vit.D3) (125mcg/ Kg) orally by gavage twice weekly. Plasma levels of lipid panel, liver enzymes, glucose, insulin, Interleukin-6 (IL-6), Interleukin-10 (IL-10), and Tumor necrosis-alpha (TNF-α)were determined. H & E staining of liver tissue were performed to assess the effects of vit.D3 treatment on olanzapine-induced histopathology. Results: Co-administration of vit.D3 caused significant elevation of IL-6, IL-10, HDL/LDL and mild improvement of liver histopathology. However, it caused further elevation of triglycerides (TGs), total cholesterol (TC), very low density lipoproteins (VLDL), TNF-α, liver enzymes, plasma, bilirubin, and impaired glucose tolerance. Insignificant difference in weight gain and abdominal fat was found. Conclusion: These results suggest that olanzapine-induced disturbed lipid profile and hepatic steatosis is independent of weight gain.Moreover, this study provides an evidence for adverse effects of vitamin D supplementation especially in patients treated with olanzapine.

Objective: Atypical antipsychotics represented a major advance in the treatment of schizophrenia and minimizing the extrapyramidal side effects. However, the use of atypical antipsychotics have been linked to weight gain, hyperglycemia, metabolic syndrome and risk of liver affection. Previous studies proposed that vitamin D deficiency may contribute to the development of insulin resistance, metabolic syndrome and more recently fatty liver. The goal of this study wasto investigate the role of vitamin D in protection against the metabolic and hepatic side effects of olanzapine. Methods: Eighteen female albino rats received treatment by gavage for 5 weeks and divided into; C group: received (0.5ml/day) of normal saline and olive oil (0.2ml) twice weekly, (O) group: received olanzapine (2mg/ kg/day) and olive oil (0.2ml) twice weekly, and (O+D) group: received olanzapine (2mg/kg/day) and vitamin D3 (vit.D3) (125mcg/ Kg) orally by gavage twice weekly. Plasma levels of lipid panel, liver enzymes, glucose, insulin, Interleukin-6 (IL-6), Interleukin-10 (IL-10), and Tumor necrosis-alpha (TNF-α)were determined. H & E staining of liver tissue were performed to assess the effects of vit.D3 treatment on olanzapine-induced histopathology. Results: Co-administration of vit.D3 caused significant elevation of IL-6, IL-10, HDL/LDL and mild improvement of liver histopathology. However, it caused further elevation of triglycerides (TGs), total cholesterol (TC), very low density lipoproteins (VLDL), TNF-α, liver enzymes, plasma, bilirubin, and impaired glucose tolerance. Insignificant difference in weight gain and abdominal fat was found. Conclusion: These results suggest that olanzapine-induced disturbed lipid profile and hepatic steatosis is independent of weight gain.Moreover, this study provides an evidence for adverse effects of vitamin D supplementation especially in patients treated with olanzapine.

Various studies have indicated that peptic ulcers occurring during the course of diabetic state are more severe and often associated with complications such as gastrointestinal bleeding. This study is an attempt to understand the pathogenesis of indomethacin-induced gastric ulcers occurring during the diabetic state using suitable markers and its amelioration by quercetin and coenzyme Q10 (CoQ10). In this study, diabetic rats showed an increase in the gastric mucosal levels of Molandialdehyde (MDA), inducible nitric oxide synthase (iNOS), interleukin-6 (IL-6), tumor necrosis factor (TNF-α), BAX and p53 and a decrease in the activities of superoxide dismutase (SOD) as compared to normal control (non-diabetic) rats. There was an increase in gastric ulcer index and gastric ulcer lesions in diabetic gastric mucosa when compared to the normal control group. Pre-treatment with quercetin andor CoQ10 to normal groups or diabetic groups which treated by indomethacin caused a significant decrease in gastric ulcer index, MDA, iNOS, IL-6, TNF-α, BAX and p53 with concomitant increase in SOD activity when compared with normal and diabetic rats treated with indomethacin alone. So quercetin and CoQ10 are effective in protection against indomethacin-induced gastric ulcers in normal and diabetic rats. Our findings could bring new hope for a novel modality of gastric ulcer treatment.

Oxytocin (OT) is well known for its role in reproduction. However, evidence has emerged suggesting a role in cardiovascular system but less is known about the role of this hormone in the injured heart. We elucidate oxytocin cardioprotective effects against myocardial infarction (MI). Male rats were divided into six groups: control without surgery, sham without occlusion, MI, OT pretreated then MI, combined OT and L-NAME (NO synthase inhibitor) then MI and combined OT and indomethacin (cyclooxygenase blocker) then MI. Twenty-four hours post-MI induction, hemodynamics parameters, inflammation markers, oxidative stress markers, apoptotic gene expression, brain naturitic peptide (BNP), and histopathological assessment were carried out. When compared to MI model group, OT significantly reduced LVEDP and increased LVSP and ± dP/dt.Also, it significantly decreased serum levels of BNP, TNF-α, IL-6, and TBARS with an increase in the activities of SOD and GPx. Furthermore, BAX and p53 mRNA were decreased. Interestingly, no significant improvement in any of the markers was detectable when we administrated OT with L-NAME. While the same results observed when we treated the rat with OT and indomethacin. We conclude that OT protected against the sequelae of myocardial infarction. These findings provide new insight into therapeutic strategies for myocardial infarction.

In the current study, we aimed to investigate the mechanistic role of DJ-1/PI3K/Akt survival pathway in ischemia/reperfusion (I/R) induced cerebral damage and to investigate if the Resveratrol (RES) mediates its ischemic neuroprotection through this pathway. RES administration to sham rats, boosted GSH level and SOD activity and downregulated iNOS expression without affecting redox levels of DJ-1 forms nor components of PI3K/Akt pathway including PTEN, p-Akt or p/p-GSK3b. However, RES pre-administration to I/R rats, reduced infarction area, oxidative stress, inflammation and apoptosis. Concomitantly, RES ameliorated the decreased levels of oxidized forms of DJ-1 and enhancing its reduction, increased the nuclear protein expression of Nfr-2 and led to activation of PI3K/Akt survival pathway. In conclusion, overoxidation of DJ-1 is a major factor that contributes to post I/R cerebral damage andits reduction by RES could explain the neuroprotection offered by RSE.

To measure tissue levels of bisphenol A (BPA) in uterine leiomyoma (ULM), adjacent myometrium (Myo-F), and normal myometrium (Myo-N). Also, we tested the effect of BPA treatment on rat myometrium. Methods: Uterine leiomyomas and Myo-F tissues were isolated from hysterectomy specimens done to treat symptomatic ULMs (N ¼ 30). Normal myometrium is isolated from hysterectomies done on ULM-free uteri for other benign indications (N ¼ 25). Bisphenol A was measured in 1 g of tissue using solid-phase extraction and high-performance liquid chromatography, with fluorescence detectors. Experimentally, adult female rats were fed BPA orally at a dose of 50 mg/kg/d for 90 days. Animals were killed, and their myometrial thickness and proliferating cell nuclear antigen (PCNA) immunostaining were evaluated. Results: Tissue concentration of BPA in each of ULM (12.3 + 2.8 mg/g) and Myo-F (10.1 + 0.2 mg/g) was significantly higher than that of Myo-N (0.58 + 0.2 mg/g). There was no statistically significant difference in BPA level between ULM and Myo-F within submucous or interstitial/subserous fibroid groups. Compared to control rats, BPA-treated animals showed significantly higher myometrial thickness (168.67+5.7 mm and 281.6+ 20.32 mm, respectively, P ¼ .003) and increased myometrial PCNA immunoscores (1.5 + 0.37 and 10.38 + 0.67, respectively, P  .001). Conclusion: Bisphenol A concentrates in human ULM tissue and its adjacent Myo-F compared to Myo-N. No significant difference is detected in BPA content of ULM tissue of different subtypes. Bisphenol A increases thickness and induces cellular proliferation in rat myometrium. Taken together, our results support a role of BPA in ULM development/growth.

To measure tissue levels of bisphenol A (BPA) in uterine leiomyoma (ULM), adjacent myometrium (Myo-F), and normal myometrium (Myo-N). Also, we tested the effect of BPA treatment on rat myometrium. Methods: Uterine leiomyomas and Myo-F tissues were isolated from hysterectomy specimens done to treat symptomatic ULMs (N ¼ 30). Normal myometrium is isolated from hysterectomies done on ULM-free uteri for other benign indications (N ¼ 25). Bisphenol A was measured in 1 g of tissue using solid-phase extraction and high-performance liquid chromatography, with fluorescence detectors. Experimentally, adult female rats were fed BPA orally at a dose of 50 mg/kg/d for 90 days. Animals were killed, and their myometrial thickness and proliferating cell nuclear antigen (PCNA) immunostaining were evaluated. Results: Tissue concentration of BPA in each of ULM (12.3 + 2.8 mg/g) and Myo-F (10.1 + 0.2 mg/g) was significantly higher than that of Myo-N (0.58 + 0.2 mg/g). There was no statistically significant difference in BPA level between ULM and Myo-F within submucous or interstitial/subserous fibroid groups. Compared to control rats, BPA-treated animals showed significantly higher myometrial thickness (168.67+5.7 mm and 281.6+ 20.32 mm, respectively, P ¼ .003) and increased myometrial PCNA immunoscores (1.5 + 0.37 and 10.38 + 0.67, respectively, P  .001). Conclusion: Bisphenol A concentrates in human ULM tissue and its adjacent Myo-F compared to Myo-N. No significant difference is detected in BPA content of ULM tissue of different subtypes. Bisphenol A increases thickness and induces cellular proliferation in rat myometrium. Taken together, our results support a role of BPA in ULM development/growth.

To measure tissue levels of bisphenol A (BPA) in uterine leiomyoma (ULM), adjacent myometrium (Myo-F), and normal myometrium (Myo-N). Also, we tested the effect of BPA treatment on rat myometrium. Methods: Uterine leiomyomas and Myo-F tissues were isolated from hysterectomy specimens done to treat symptomatic ULMs (N ¼ 30). Normal myometrium is isolated from hysterectomies done on ULM-free uteri for other benign indications (N ¼ 25). Bisphenol A was measured in 1 g of tissue using solid-phase extraction and high-performance liquid chromatography, with fluorescence detectors. Experimentally, adult female rats were fed BPA orally at a dose of 50 mg/kg/d for 90 days. Animals were killed, and their myometrial thickness and proliferating cell nuclear antigen (PCNA) immunostaining were evaluated. Results: Tissue concentration of BPA in each of ULM (12.3 + 2.8 mg/g) and Myo-F (10.1 + 0.2 mg/g) was significantly higher than that of Myo-N (0.58 + 0.2 mg/g). There was no statistically significant difference in BPA level between ULM and Myo-F within submucous or interstitial/subserous fibroid groups. Compared to control rats, BPA-treated animals showed significantly higher myometrial thickness (168.67+5.7 mm and 281.6+ 20.32 mm, respectively, P ¼ .003) and increased myometrial PCNA immunoscores (1.5 + 0.37 and 10.38 + 0.67, respectively, P  .001). Conclusion: Bisphenol A concentrates in human ULM tissue and its adjacent Myo-F compared to Myo-N. No significant difference is detected in BPA content of ULM tissue of different subtypes. Bisphenol A increases thickness and induces cellular proliferation in rat myometrium. Taken together, our results support a role of BPA in ULM development/growth.

To measure tissue levels of bisphenol A (BPA) in uterine leiomyoma (ULM), adjacent myometrium (Myo-F), and normal myometrium (Myo-N). Also, we tested the effect of BPA treatment on rat myometrium. Methods: Uterine leiomyomas and Myo-F tissues were isolated from hysterectomy specimens done to treat symptomatic ULMs (N ¼ 30). Normal myometrium is isolated from hysterectomies done on ULM-free uteri for other benign indications (N ¼ 25). Bisphenol A was measured in 1 g of tissue using solid-phase extraction and high-performance liquid chromatography, with fluorescence detectors. Experimentally, adult female rats were fed BPA orally at a dose of 50 mg/kg/d for 90 days. Animals were killed, and their myometrial thickness and proliferating cell nuclear antigen (PCNA) immunostaining were evaluated. Results: Tissue concentration of BPA in each of ULM (12.3 + 2.8 mg/g) and Myo-F (10.1 + 0.2 mg/g) was significantly higher than that of Myo-N (0.58 + 0.2 mg/g). There was no statistically significant difference in BPA level between ULM and Myo-F within submucous or interstitial/subserous fibroid groups. Compared to control rats, BPA-treated animals showed significantly higher myometrial thickness (168.67+5.7 mm and 281.6+ 20.32 mm, respectively, P ¼ .003) and increased myometrial PCNA immunoscores (1.5 + 0.37 and 10.38 + 0.67, respectively, P  .001). Conclusion: Bisphenol A concentrates in human ULM tissue and its adjacent Myo-F compared to Myo-N. No significant difference is detected in BPA content of ULM tissue of different subtypes. Bisphenol A increases thickness and induces cellular proliferation in rat myometrium. Taken together, our results support a role of BPA in ULM development/growth.

To measure tissue levels of bisphenol A (BPA) in uterine leiomyoma (ULM), adjacent myometrium (Myo-F), and normal myometrium (Myo-N). Also, we tested the effect of BPA treatment on rat myometrium. Methods: Uterine leiomyomas and Myo-F tissues were isolated from hysterectomy specimens done to treat symptomatic ULMs (N ¼ 30). Normal myometrium is isolated from hysterectomies done on ULM-free uteri for other benign indications (N ¼ 25). Bisphenol A was measured in 1 g of tissue using solid-phase extraction and high-performance liquid chromatography, with fluorescence detectors. Experimentally, adult female rats were fed BPA orally at a dose of 50 mg/kg/d for 90 days. Animals were killed, and their myometrial thickness and proliferating cell nuclear antigen (PCNA) immunostaining were evaluated. Results: Tissue concentration of BPA in each of ULM (12.3 + 2.8 mg/g) and Myo-F (10.1 + 0.2 mg/g) was significantly higher than that of Myo-N (0.58 + 0.2 mg/g). There was no statistically significant difference in BPA level between ULM and Myo-F within submucous or interstitial/subserous fibroid groups. Compared to control rats, BPA-treated animals showed significantly higher myometrial thickness (168.67+5.7 mm and 281.6+ 20.32 mm, respectively, P ¼ .003) and increased myometrial PCNA immunoscores (1.5 + 0.37 and 10.38 + 0.67, respectively, P  .001). Conclusion: Bisphenol A concentrates in human ULM tissue and its adjacent Myo-F compared to Myo-N. No significant difference is detected in BPA content of ULM tissue of different subtypes. Bisphenol A increases thickness and induces cellular proliferation in rat myometrium. Taken together, our results support a role of BPA in ULM development/growth.