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Aim: Menopause is defined as the depletion of the ovarian follicular reserve followed by the cessation of menstrual cycles. It has been reported that gonadal steroid hormones play an important role in bladder function in women. Changes in urine pattern including overactive bladder, stress incontinence and recurrent urinary tract infections occur as a result of menopause. 1,1-dimethylbiguanide hydrochloride, metformin, (MET) is an oral anti-diabetic drug used to reduce hepatic glucose production and peripheral insulin resistance. Recent studies have revealed that MET has a protective effects in diabetes induced bladder dysfunction. The aim of this study was to test the therapeutic potential of MET in detrusor contractile function of ovariectomized (OVX) female rats. Material and Methods: Bilateral ovariectomy was performed to eliminate endogenous gonadal steroids secretion. Four groups are designed with 8 animals in each group: Control, MET-administered control, OVX, and MET-administered OVX groups. MET (25 mg/ kg) was administered daily by oral gavage for 14 days. Contractile activity of isolated bladder muscle strips were evaluated in vitro organ bath. The contractile responses of detrusor strips were determined using different doses of carbachol (10-8-10-2M) and purinergic agonist ATP. The relaxation response of strips were determined by isoproterenol Results: The contractile responses of detrusor muscle strips to carbachol at doses 10-5-10-2 M were decreased in the OVX group compared to control and MET treated control groups. MET treatment partially reversed the reduction in OVX-induced contractile responses at 10-2 and 10 -3 M carbachol doses. There were no statistically significant difference in relaxation response between the experimental groups. Conclusion: Our findings suggest that treatment with MET could be the new potential therapeutic agent against bladder dyfunction in postmenopausal women. Further studies are needed for the therapeutic potential of MET in detrusor dysfunction induced by menopause.

Several studies have shown that low estrogen levels can lead to an increase in the incidence of depression and anxiety during menopause. The hippocampus and prefrontal cortex are parts of the brain involved in depressive- and anxiety-like behaviors. Recent studies have revealed that metformin has neuroprotective effects mainly due to its antioxidant properties. The aim of the present study was to examine the therapeutic potential of metformin in depressive- and anxiety-like behavior as well as oxidative stress in the prefrontal cortex and hippocampus of ovariectomized rats. Young female Wistar Albino rats were distributed into four groups (n:8): control, metformin-administered control, ovariectomized and metformin administered ovariectomized groups. Metformin (25 mg/kg) was administered daily by oral gavage for 2 weeks. Forced swimming test and open field test were performed to evaluate depression- and anxiety-like behaviors, respectively. Following the treatment with metformin, the tissues of the hippocampus and prefrontal cortex were isolated for the measurement of malondialdehyde, reduced glutathione and ascorbic acid contents. Ovariectomy resulted in depressive- and anxiety-like behaviors, and besides, increased content of malondialdehyde in both prefrontal cortex and hippocampus. The levels of ascorbic acid and glutathione were found to be reduced in ovariectomized rats. Metformin treatment significantly decreased depressive behaviour and malondialdehyde content in the prefrontal cortex. Reducing oxidative stress of the prefrontal cortex was suggested as a possible mechanism implicated in the beneficial effects of metformin on ovariectomy-induced depressive-like behaviour. We believe that the therapeutic efficiency of metformin needs to be tested for potential clinical use in surgical menopause or gonadal hormone deficiency women with depression.

Aim: Intestinal ischemia/reperfusion (I/R) produces multiple organ injury including lung. Pulmonary tissue damage and respiratory failure are prevalent events after intestinal ischemia. It is generally known that oxidative stress mediators such as reactive oxygen species (ROS) is believed to have a role in the development of such I/R-induced pulmonary injury. Under the light of these data, the aim of the present study was to investigate whether metformin treatment would alleviate the acute lung injury induced by intestinal I/R in rats, histolopathologically and biochemically. Material and Methods: A rat model of intestinal I/R was induced by clamping the superior mesenteric artery for 45 min followed by reperfusion for three hours. Metformin was administrated orally five days before intestinal ischemia (50,100 or 200 mg/kg). Forty