Protective effect and mechanism of cryptotanshinone on kidney of rats with STZ-induced diabetic nephropathy
Objective To explore the effects and possible action mechanisms of cryptotanshinone on kidney in rats with diabetic nephropathy(DN)induced by streptozotocin(STZ).Methods According to random number table method,60 rats were divided into control group,DN model group,low-dose,medium-dose and high-dose cryptotanshinone groups(15,30,60 mg·kg-1·d-1),and metformin group(200 mg·kg-1·d-1).Except for control group,rats in the other groups were induced by STZ to prepare DN rat models.At 24h after the end of administration,plasma glucose(FPG),triglyceride(TG),total cholesterol(TC),low-density lipoprotein cholesterol(LDL-C),high-density lipoprotein cholesterol(HDL-C),24h urine protein quantification,blood urea nitrogen(BUN),serum creatinine(Scr),superoxide dismutase(SOD),malondialdehyde(MDA)and reactive oxygen species(ROS)were detected.The expression levels of proteins related to TGF-β1/Smad3 signaling pathways were detected by Western blot.Results The detection results of biochemical indexes showed that after drug intervention,levels of FPG,urine protein,BUN,Scr,MDA,ROS,TG,TC,LDL-C,high-shear,mid-shear and low-shear viscosity,and plasma viscosity in metformin group,medium-dose and high-dose cryptotanshinone groups were lower than those in DN model group,while levels of SOD and HDL-C were higher than those in DN model group.The results of Western blot showed that after drug intervention,expression level of TGF-β1 protein and p-Smad3/Smad3 ratio in metformin group,medium-dose and high-dose cryptotanshinone groups were lower than those in DN model group,while p-Smad7/Smad7 ratio was higher than that in the DN model group.Conclusion Cryptotanshinone can improve glucose-lipid metabolism,oxidative stress and hemorheology in rats with STZ-induced DN,and enhance their renal function.The protective mechanisms may be related to activating TGF-β1/Smad3 signaling pathways.
diabetic nephropathycryptotanshinoneTGF-β1/Smad3 signaling pathwayoxidative stresshyperlipidemiarat model