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کاربرد نوع شرط:
- جایگاه : پژوهشی
- مجله: Iranian Journal of Basic Medical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: Gene expression,Gestational Diabetes Mellitus,Langerhans islets,Offspring
- چکیده:
- چکیده انگلیسی: Objective(s): The link between a hyperglycemic intrauterine environment and the development of diabetes later in life has been observed in offspring exposed to gestational diabetes mellitus (GDM), but the underlying mechanisms for this phenomenon are still not clear. Reduced β-cells mass is a determinant in the development of diabetes (type 1 and type 2 diabetes). Some recent studies have provided evidence that the CDK4-pRB-E2F1 regulatory pathway is involved in β-cells proliferation. Therefore, we postulated that GDM exposure impacts the offspring’s β-cells by disruption in the CDK4-pRB-E2F1 pathway.
Materials and Methods: Adult Wistar rats were randomly allocated in control and diabetic group. The experimental group received 40 mg/kg/body weight of streptozotocin (STZ) on day zero of gestation. After delivery, diabetic offspring of GDM mothers and control dams at the age of 15 week were randomly scarified and pancreases were harvested. Langerhans islets of diabetic and control groups were digested by collagenase digestion technique. After RNA extraction, we investigated the expressions of the kir 6.2 and CDK4-pRB-E2F1 pathway genes by quantitative real-time PCR.
Results: GDM reduced the expression of CDK4-pRB-E2F1 pathway genes in Langerhans islets cells of offspring. CDK4, pRB and E2F1 pathway genes were downregulated in diabetic islets by 51%, 35% and 84%, respectively. Also, the expression of Kir 6.2 was significantly decreased in diabetic islets by 88%.
Conclusion: We suggest that the effect of gestational diabetes on offspring’s β-cells may be primarily caused by the suppression of CDK4-pRB-E2F1 pathway.- انتشار مقاله: 12-11-1395
- نویسندگان: Zahra Nazari,Mohammad Nabiuni,Mohsen Saeidi,Mohammad Jafar Golalipour
- مشاهده
- جایگاه : پژوهشی
- مجله: Advanced Herbal Medicine
- نوع مقاله: Journal Article
- کلمات کلیدی: Urtica dioica,Polycystic Ovary Syndrome,Liver,Necrosis,Insulin resistance
- چکیده:
- چکیده انگلیسی: Background and aims: Urtica dioica as a medicinal herb due to its anti-inflammatory, antioxidant and hypoglycemic effects, improve type 2 diabetes and decrease inflammation, fibrosis and necrosis as the signs of Nonalcoholic steatohepatitis. Polycystic Ovary Syndrome (PCOS) as the most important factor of infertility has an overlap of 30 % to 60% with liver disorders. Hence, the Urtica dioica moderator effect on liver function in PCOS rats was examined. Methods: In this experimental study 144 adult Wistar rats were divided into control, PCOS and nettle-treated groups. The group PCOS was injected subcutaneously 2 mg estradiol valerate, after 60 days and confirmed polycystic, the experimental group was injected intraperitoneally the Urtica dioica extract doses (150,250, 450 mg/kg BW). After 21 days, rats were anesthetized by chloroform; blood samples and livers were collected for histological and serological evaluation. Data were analyzed using instat3 via ANOVA one-way and p
- انتشار مقاله: 19-11-1393
- نویسندگان: Samad Zare,Mohammad Nabiuni,Akram Tayanloo,Serwa Hoseini,Latifeh Karimzadeh-Bardei
- مشاهده