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Scholars Academic Journal of Biosciences | Volume-2 | Issue-09
Asymetric Dimethylarginine Levels and Dimethylarginine Dimethylaminohidrolase 2 Expression on Nitric Oxide Synthesis Pathway in Sprague Dawley Rats Induced Nicotinamide and Streptozotocin by Giving Physalis angulata L
Yeny Sulistyowati, Sri Kadarsih Soedjono, Mustofa, Budi Mulyono
Published: Dec. 30, 2014 | 185 122
DOI: 10.36347/sajb.2014.v02i09.004
Pages: 577-582
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Abstract
Hyperglycemia in patients with diabetes will increase oxidative stress to the endothelium and cause endothelial dysfunction. Endothelial dysfunction related to oxidative stress due to hyperglycemia can be improved through several mechanisms, including the synthesis of nitric oxide pathway (NO). Physalis angulata L is one kind of plant that has been used as an antidiabetic, due to fisalin. The Objective of this study is to determine the levels of Asymetric Dhymetilarginine (ADMA) and expression Dhymethilamine Dehidrolase 2 (DDAH2) on Nitric Oxide (NO) synthesis pathway in Sprague Dawley rats induced Nicotinamide (NIC) - Streptozotocin (STZ) by giving P. angulata L standardized fisalin. The study was true experimental research design with a post-test only control group design. Subjects were 30 male Sprague-Dawley rats induced STZ (45 mg/BW) and NIC (110 mg/BW). Giving P. angulata L standardized fisalin with a dose of 20 mg/BW was conducted for 21 days. Insulin injections of 200 mg/BW and verapamil injections of 1 mg/BW. It is found that there was a significant result (p = 0.009; r = 0.596 and R2 = 0.355) and the effect of variation of 35.5% of the group ADMA levels. There was a significant result (p = 0.004; r = 0.505 and R2 = 0.255) and the effect of variation was 25.5% of the group DDAH2 expression in circular position and there was no effect (p = 0.284; R = 0.202 and R2 = 0.041) on the expression of group variation DDAH2 longitudinal position. In conclusion, giving of P. angulata L standardized fisalin can improve NO synthesis through a decrease in ADMA levels and increased expression of DDAH2.