Ney of diabetic rats. The expression Nelarabine Arranon of these components were consistent with verst Markets MDA, which is a marker of lipid peroxidation induced ROS increased ht And reduced activity of GPx-t, the antioxidant defense system. All these compounds Changes were prepared by treatment of curcumin, which has been demonstrated that oxidative stress is normalized to be prevented by inhibition of PKC activity t. In agreement, others have shown that curcumin diabetes-induced decrease of antioxidant capacity T in the retina and the kidney to prevent. The concentration of curcumin used in this study K Body weight was 100 mg / kg. A Similar dose of curcumin was found to be effective in preventing kidney disease and decreased cellular Ren oxidative stress and reduced blood levels of proinflammatory cytokines in animal experiments. This dose is equivalent to 6 g per adult, provided, 60 kg K Body weight per adult, and has been used in humans. In summary, our results show that curcumin protects against the development of DN, double blocking activity Th of the two classical PKC isoforms, PKC and PKC a B1 and downstream Means rts of ERK1 / 2. In addition, the results of this study suggest that the main mechanism involved in the anti-fibrotic curcumin’s potent antioxidant property. Because of its excellent safety profile and a long history of use S Re, curcumin may find clinical application in the prevention of complications in diabetic patients. CYP7A1 gene expression and bile from the liver Uresynthese show a clear circadian rhythm. In rodents, the bile Acid synthesis and CYP7A1 expression in the dark period peaked and declined in the light period. In humans, CYP7A1 activity
-t, as indicated by the marking of bile Acid synthesis of serum 7 is hydroxy-4 cholesten 3-level one, a double peak, Co Ncider with food intake, demonstrated reduced at night, and a return to baseline values in the morning. Because hepatic metabolism is very active may need during the postprandial period, and the human experience I To do that power cycles several times a day, these observations indicate an m Adjusted association between induction of the synthesis of bile Acids and the regulation of postprandial N Drastic decrease metabolism. Therefore, it is likely that the N Hrstoffzufuhr synthesis of bile Acid regulates w During bile Acid contr L postprandial absorption of N Nutrients and metabolism. Unfortunately, a clear proof of the scheme of N Drastic decrease metabolism of bile Acids in the liver or from. It was reported that bile acids And f Kale Gallen Acid pool in diabetic patients with hyperglycemia Chemistry uncontrollably EEA erh Ht and are w Reduced during treatment with insulin. CYP7A1 activity, t is increased in streptozotocin-diabetic rats Ht, suggesting that insulin suppresses CYP7A1, w While a lack of insulin induced CYP7A1. In addition, it was reported that peroxisome proliferator-activated receptor coactivator 1 transcription of the CYP7A1 gene in M Nozzles after a night I Parts selected. In contrast to these studies to M Mice, we reported that insulin and glucose, w While glucagon induced CYP7A1 gene suppressed in the primary Ren human hepatocytes. It was assumed that species differences in the regulation of gene transcription of human and rodent CYP7A1 k Nnte the observed discrepancy explained Ren. In this study, we have a humanized CYP7A1 transgenic mouse model.