Pyritinol reduces nociception and oxidative stress in diabetic rats

2008 ◽  
Vol 590 (1-3) ◽  
pp. 170-176 ◽  
Author(s):  
Guillermina Yanek Jiménez-Andrade ◽  
Gerardo Reyes-García ◽  
Gabriela Sereno ◽  
Guillermo Ceballos-Reyes ◽  
Guadalupe C. Vidal-Cantú ◽  
...  
Author(s):  
Basiru Olaitan Ajiboye ◽  
Babatunji Emmanuel Oyinloye ◽  
Jennifer Chidera Awurum ◽  
Sunday Amos Onikanni ◽  
Adedotun Adefolalu ◽  
...  

Abstract Objectives The current study evaluates the protective role of aqueous extract of Sterculia tragacantha leaf (AESTL) on pancreatic gene expressions (insulin, PCNA, PDX-1, KI-67 and GLP-1R) and oxidative stress parameters in streptozotocin-induced diabetic rats. Methods Diabetes mellitus was induced into the experimental Wistar animals via intraperitoneal (IP) injection of streptozotocin (35 mg/kg body weight) and 5% glucose water was given to the rats for 24 h after induction. The animals were categorized into five groups of 10 rats each as follows normal control, diabetic control, diabetic rats administered AESTL (150 and 300 mg/kg body weight) and diabetic rats administered metformin (200 mg/kg) orally for two weeks. Thereafter, the animals were euthanized, blood sample collected, pancreas harvested and some pancreatic gene expressions (such as insulin, PCNA, PDX-1, KI-67, and GLP-1R)s as well as oxidative stress parameters were analyzed. Results The results revealed that AESTL significantly (p<0.05) reduced fasting blood glucose level, food and water intake, and lipid peroxidation in diabetic rats. Diabetic rats administered different doses of AESTL showed a substantial upsurge in body weight, antioxidant enzyme activities, and pancreatic gene expressions (insulin, PCNA, PDX-1, KI-67, and GLP-1R). Conclusions It can therefore be concluded that AESTL has the ability to protect the pancreas during diabetes mellitus conditions.


2016 ◽  
Vol 32 (3) ◽  
pp. 329-336 ◽  
Author(s):  
Abolfazl Nasiri ◽  
Nasrin Ziamajidi ◽  
Roghayeh Abbasalipourkabir ◽  
Mohammad Taghi Goodarzi ◽  
Massoud Saidijam ◽  
...  

Author(s):  
Amal J. Fatani ◽  
Salim S. Al-Rejaie ◽  
Hatem M. Abuohashish ◽  
Abdullah Al-Assaf ◽  
Mihir Y. Parmar ◽  
...  

2014 ◽  
Vol 70 (3) ◽  
pp. 713-723 ◽  
Author(s):  
Mohamed Salah Allagui ◽  
Anouer Feriani ◽  
Zouhour Bouoni ◽  
Hichem Alimi ◽  
Jean Claud Murat ◽  
...  

Renal Failure ◽  
2015 ◽  
Vol 37 (2) ◽  
pp. 192-197 ◽  
Author(s):  
Aydın Güçlü ◽  
Nilüfer Yonguç ◽  
Yavuz Dodurga ◽  
Gülşah Gündoğdu ◽  
Zuhal Güçlü ◽  
...  

2018 ◽  
Vol 38 (2) ◽  
Author(s):  
Qian Zhang ◽  
Xinhua Xiao ◽  
Jia Zheng ◽  
Ming Li ◽  
Miao Yu ◽  
...  

Increasing evidence shows that diabetes causes cardiac dysfunction. We hypothesized that a glucagon-like peptide-1 (GLP-1) analog, liraglutide, would attenuate cardiac dysfunction in diabetic rats. A total of 24 Sprague–Dawley (SD) rats were divided into two groups fed either a normal diet (normal, n=6) or a high-fat diet (HFD, n=18) for 4 weeks. Then, the HFD rats were injected with streptozotocin (STZ) to create a diabetic rat model. Diabetic rats were divided into three subgroups receiving vehicle (diabetic, n=6), a low dose of liraglutide (Llirag, 0.2 mg/kg/day, n=6), or a high dose of liraglutide (Hlirag, 0.4 mg/kg/day, n=6). Metabolic parameters, systolic blood pressure (SBP), heart rate (HR), left ventricular (LV) function, and whole genome expression of the heart were determined. Diabetic rats developed insulin resistance, increased blood lipid levels and oxidative stress, and impaired LV function, serum adiponectin, nitric oxide (NO). Liraglutide improved insulin resistance, serum adiponectin, NO, HR, and LV function and reduced blood triglyceride (TG), total cholesterol (TC) levels, and oxidative stress. Moreover, liraglutide increased heart nuclear receptor subfamily 1, group H, member 3 (Nr1h3), peroxisome proliferator activated receptor (Ppar) α (Pparα), and Srebp expression and reduced diacylglycerol O-acyltransferase 1 (Dgat) and angiopoietin-like 3 (Angptl3) expression. Liraglutide prevented cardiac dysfunction by activating the PPARα pathway to inhibit Dgat expression and oxidative stress in diabetic rats.


2020 ◽  
Vol 12 (10) ◽  
pp. 1215-1220
Author(s):  
Bingshuang Xue ◽  
Yi Xue ◽  
Jiaojiao Zhou ◽  
Qichao Yang

The occurrence of complications of diabetic patients not only increases the difficulty and burden of treatment but also significantly affects the health and safety of patients. Traditional therapeutic drugs are prone to drug resistance, which affects the therapeutic effect. In recent years, the application of plant-derived natural compounds in the treatment of diseases has become a hot spot in the research of diabetes drugs. Curcumin has anti-tumor, anti-inflammation, anti-oxidation and antimicrobial effects, but the mechanism of its effect on cardiomyocytes in diabetic patients is not yet clear. In this study, curcumin was prepared into nano-preparations and its mechanism of action in the process of myocardial fibrosis in diabetic rats was further explored. We found that injection of curcumin nano-suspension can increase the LVIDd and LVFS of rats, while reducing the serum CKMB, LDH, AST and cTnI levels. Further exploration found that curcumin can reduce serum TNF- α and IL-1 β levels in diabetic rats, while increasing the SOD and GSH-Px activities of myocardial tissue, and reducing MDA content. These suggests that curcumin can reduce inflammation and oxidative stress in diabetic rats. Therefore, this study believes that curcumin nano-suspension can effectively inhibit diabetic cardiomyocyte fibrosis, oxidative stress, and inflammation and protect the rat myocardium.


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