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The aim of this study was to evaluate, for the first time, the antidiabetic effect of the alkaloids extract of Salvia chudaei Batt. & Trab. (Lamiaceae) on alloxan-induced diabetic rats. The alkaloids extract was prepared, and the in vitro inhibitory effect of key digesting enzymes related to postprandial hyperglycemia were determined. After acute toxicity test, the Swiss albino rats were induced with alloxan to get experimental diabetes animals. The fasting mean blood glucose, lipid profile, different liver and kidney function biomarkers and antioxidant biomarkers levels, after treatment for 30 days, diabetic untreated and diabetic rats treated with alkaloids extract were estimated. The alkaloids displayed remarkable in inhibiting α-glucosidase (IC50 = 248.25±2.61 μg/ml) than α-amylase (IC50 = 262.96±9.64 μg/ml) activities. In vivo, the results proved that alkaloids extract at dose of 500 mg/kg bw decreased significantly the blood glucose, lipid profile levels and improved the liver and kidney function biomarkers and increased the activities of antioxidant enzymes (superoxide dismutase and gluthatione reductase). This study demonstrates, that alkaloids are effective in inhibiting hyperglycemia and oxidative stress caused by diabetes.

The distribution of atrial natriuretic peptide (ANP) in blood plasma and cardiac muscle and its effects on ventricular myocyte contraction and intracellular free calcium concentration [Ca2+]i in the streptozotocin (STZ)-induced diabetic rat have been investigated. Blood plasma concentration and heart atrial and ventricular contents of ANP were significantly increased in STZ-treated rats compared to age-matched controls. STZ treatment increased the number of ventricular myocytes immunolabeled with antibodies against ANP. In control myocytes the percentage of cells that labeled positively and negatively were 17% versus 83%, respectively. However, in myocytes from STZ-treated rat the percentages were 52% versus 53%. Time to peak (TPK) shortening was significantly and characteristically prolonged in myocytes from STZ-treated rats (360+/-5 ms) compared to controls (305+/-5 ms). Amplitude of the Ca2+ transient was significantly increased in myocytes from STZ-treated rats compared to controls (0.39+/-0.02 versus 0.29+/-0.02 fura-2 RU in controls) and treatment with ANP reduced the amplitude of the Ca2+ transient to control levels. ANP may have a protective role in STZ-induced diabetic rat heart.