In the face of escalating maternal and fetal health threats, hypertensive pregnancy disorders (HPDs) is one of the leading cause of maternal and fetal morbidity and mortality. The range of HPDs include white-coat hypertension, chronic hypertension, gestational hypertension, mild-to-moderate and severe preeclampsia and eclampsia. Current evidence implicates an imbalance of circulating anti- and angiogenic factors in HPDs emanating from the placental vasculature, impacting on angiogenesis. Delivery of the fetus is thus far the only curative measure, albeit with increased risk. Resultant endothelial dysfunction caused by the excessive production of placental soluble fms-like tyrosine kinase-1 has been the basis of many studies to find a safer treatment strategy. Metformin, used historically in the treatment of diabetes mellitus has also found its therapeutic reach in many other disease states. These include, but are not limited to, improving blood flow in certain cancer types, treatment of polycystic ovarian disease, improving vasodilation, and reducing inflammation. Metformin is used to treat hyperglycemic endothelial dysfunction through the enhancement of the nitric oxide system, endothelin-derived hyperpolarizing factor and sirtuin 1. Similarly, endothelial dysfunction in preeclampsia and other HPDs leads to a hypoxic state and elevated blood pressures. Dubbed as the new "aspirin" of current times, the retardation of the antiangiogenic status by metformin provides an exciting and promising alternate strategy in treating these pregnancy disorders.

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Manic episode in bipolar disorder (BD) was evaluated in the present study with supplementation of omega-3 fatty acids in combination with aripiprazole and lithium on methylphenidate (MPD)-induced manic mice model. Administration of MPD 5 mg/kg bw intraperitoneally (i.p.) caused increase in oxidative stress in mice brain. To retract this effect, supplementation of omega-3 fatty acids 1.5 ml/kg (p.o.), aripiprazole 1.5 mg/kg bw (i.p.), and lithium 50 mg/kg bw (p.o) were given to mice. Omega-3 fatty acids alone and in combination with aripiprazole- and lithium-treated groups significantly reduced the levels of superoxide dismutase (SOD), catalase (CAT), and lipid peroxidation products (thiobarbituric acid reactive substances) in the brain. MPD treatment significantly decreased the reduced glutathione (GSH) level and glutathione peroxidase (GPx) activity, and they were restored by supplementation of omega-3 fatty acids with aripiprazole and lithium. There is no remarkable difference in the effect of creatine kinase (CK) activity between MPD-induced manic model and the treatment groups. Therefore, our results demonstrate that oxidative stress imbalance and mild insignificant CK alterations induced by administration of MPD can be restored back to normal physiological levels through omega-3 fatty acids combined with lithium and aripiprazole that attributes to effective prevention against mania in adult male Swiss albino mice.

Aim: Chronic renal failure (CRF) is one of the major contributors of cardiovascular pathological events and CRF associated uremic condition in rats elevates liver oxidative stress. The aim of the present study was to evaluate the preventive potential of diosgenin on antioxidant system and molecular protection potential in liver of CRF rats. Materials and Methods: CRF in rats was induced by feeding rats with diet containing 0.75% adenine for 5 weeks. Diosgenin was given orally at a dose of 40 mg/kg body weight (bw) of animal each and every day. The activities of antioxidant enzymes and lipid peroxidation level were determined by biochemical assays. Fourier transform infrared spectroscopy (FTIR) was employed to illustrate the molecular protection potential of diosgenin. Results: This study has shown adenine containing diet induced CRF in rats elevates liver oxidative stress by suppressing the activity of enzymatic antioxidant system, increased lipid peroxidation, and macromolecular structural alterations. In this study, treatment of diosgenin 40 mg/kg bw of rat signifi cantly restores the enzymatic antioxidant system and reduces the lipid peroxidation level. Moreover, based on the FTIR study, we confi rmed that diosgenin administration signifi cantly protected the macromolecular changes including, the protein structural damage that occurred in liver. Conclusion: This study has proved the hepato protective action of diosgenin through antioxidant and molecular protection effect in CRF condition.