Baicalin improves renal fibrosis in rats with chronic kidney disease by regulating the galectin-3/Akt/GSK-3β/Snail signaling pathway
Objective To investigate the impact of baicalin on renal fibrosis in rats with chronic kidney disease by regulating the galectin-3/protein kinase B(Akt)/glycogen synthase kinase(GSK-3β)/Snail signaling pathway.Methods The renal fibrosis model in rats with chronic kidney disease was created by adenine induction.The healthy male Sprague-Dawley(SD)rats were randomly grouped into control group,model group,positive drug group(treatment of losartan 9mg/kg),low-dose baicalin group(treatment of baicalin 20mg/kg),medium-dose baicalin group(treatment of baicalin 40mg/kg),and high-dose baicalin group(treatment of baicalin 80mg/kg).Drug administration was given through oral gavage,and rats in the model group and control group were given an equal volume of normal saline by gavage.After 30 days,serum urea nitrogen(BUN)and serum creatinine(Scr)levels of rats were measured.The collagen distribution area of kidney tissues was measured by Masson staining.Pathological changes of kidney tissues were observed by hematoxylin & eosin(H&E)staining.Positive expressions of α-smooth muscle actin(α-SMA)and type Ⅰ collagen A1(CoLIA1)in kidney tissues were detected by immunohistochemistry.Western blot was applied to analyze the protein expressions of galactin-3,p-Akt/Akt,p-GSK-3β/GSK-3β and Snail in kidney tissues.Results Compared with the control group,rats in the model group had severe renal injury,deposition of black adenine metabolite crystals,significantly increased collagen fibers,enlarged collagen distribution area of kidney tissues,and upregulated α-SMA,CoLIA1,Scr,BUN,galectin-3,p-Akt/Akt,p-GSK-3β/GSK-3β,and Snail(P＜0.05).Compared with the model group,the pathological changes of renal interstitium,glomerulus and renal tubule in the positive drug group,low-dose,medium-dose and high-dose baicalin group were significantly alleviated,with the significantly reduced crystallization of adenine metabolites and fibrotic tissues,smaller collagen distribution area of kidney tissues,and downregulated α-SMA,CoLIA1,Scr,BUN,galectin-3,p-Akt/Akt,p-GSK-3β/GSK-3β,and Snail(P＜0.05).Conclusion Baicalin improves renal fibrosis in rats with chronic kidney disease by inhibiting the galectin-3/Akt/GSK3β/Snail signaling pathway.
baicalinchronic kidney diseaserenal fibrosisgalectin-3/protein kinase B/glycogen synthase kinase/Snail signal pathway
万方数据
维普
