Streptozotocin-induced diabetes increases apoptosis through JNK phosphorylation and Bax activation in rat testes.
نویسنده
چکیده
Diabetic disease is known to suppress male reproductive activity in laboratory animals and humans. The present study was designed to evaluate whether streptozotocin-induced diabetes increases apoptotic cell death in rat testes through activation of the JNK and Bax pathway. Diabetes was induced by a single intravenous injection of streptozotocin (40 mg/kg) and testis samples were collected after 3 months. Compared with controls, body weight and testicular weight were lower in the diabetic group, and the apoptotic index in testicular germ cells was significantly increased. Expression of phospho-JNK and Bax was significantly increased in the diabetic group, and the level of activated caspase-3 was also increased, compared to that of controls. Our findings suggest that streptozotocin-induced diabetes increases apoptotic cell death in rat testes through phosphorylation of JNK and activation of Bax.
منابع مشابه
Inhibition of JNK by compound C66 prevents pathological changes of the aorta in STZ-induced diabetes
Cardiovascular diseases as leading causes of the mortality world-wide are related to diabetes. The present study was to explore the protective effect of curcumin analogue C66 on diabetes-induced pathogenic changes of aortas. Diabetes was induced in male C57BL/6 mice with a single intraperitoneal injection of streptozotocin. Diabetic mice and age-matched non-diabetic mice were randomly treated w...
متن کاملMatrine inhibits diethylnitrosamine-induced HCC proliferation in rats through inducing apoptosis via p53, Bax-dependent caspase-3 activation pathway and down-regulating MLCK overexpression
The proliferation of hepatocellular carcinoma (HCC) cells is one of the leading causes of liver cancer mortality in humans. The inhibiting effects of matrine on HCC cell proliferation have been studied, but the mechanism of that inhibition has not been fully elucidated. Since, apoptosis plays an important role in HCC cell proliferation. We examined the apoptosis-inducing effect of matrine on tu...
متن کاملMatrine inhibits diethylnitrosamine-induced HCC proliferation in rats through inducing apoptosis via p53, Bax-dependent caspase-3 activation pathway and down-regulating MLCK overexpression
The proliferation of hepatocellular carcinoma (HCC) cells is one of the leading causes of liver cancer mortality in humans. The inhibiting effects of matrine on HCC cell proliferation have been studied, but the mechanism of that inhibition has not been fully elucidated. Since, apoptosis plays an important role in HCC cell proliferation. We examined the apoptosis-inducing effect of matrine on tu...
متن کاملP-18: Effect of Royal Jelly on Oxidative Stress Marker in Testes Tissue in Streptozotocin-Induced Diabetic Rat
Background: Chronic diabetes mellitus is accompanied with enhanced oxidative stress and reduce the activity of antioxidant defense system. Due to significant role of enhanced oxidative stress in development of testes damage in diabetices, this study was conducted to evaluate the effect of royal jelly on oxidative stress marker in testis tissue of diabetic rats. Materials and Methods: In this ex...
متن کاملJNK promotes Bax translocation to mitochondria through phosphorylation of 14-3-3 proteins.
Targeted gene disruption studies have established that the c-Jun NH2-terminal kinase (JNK) is required for the stress-induced release of mitochondrial cytochrome c and apoptosis, and that the Bax subfamily of Bcl-2-related proteins is essential for JNK-dependent apoptosis. However, the mechanism by which JNK regulates Bax has remained unsolved. Here we demonstrate that activated JNK promotes Ba...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید
ثبت ناماگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید
ورودعنوان ژورنال:
- The Journal of veterinary medical science
دوره 69 9 شماره
صفحات -
تاریخ انتشار 2007