Study on the effects of triptolide on the expression of glucose transporter-1 (GLUT-1) mRNA in renal cortex of the diabetic rats

Objective To investigate the effects of triptolide on the expression of glucose transporter(GLUT)-1 mRNA in the diabetic kidneys,and probe into its mechanism.Methods The rat diabetes model was established by intraperitoneal injection of STZ.Forty-six adult Wistar rats(half males and half females),3 months old,were divided randomly into normal control,diabetic model and triptolide treated groups(6.7 mg·kg-1·d-1).Four rats of each group were sacrificed at the end of the 4th,8th,12th week to collect samples for recordingbody weight,right kidney weight,blood sugar,serum creatinine,blood urea nitrogen,24-hour urinary protein excretion.Renal GLUT-1 mRNA expression was measured with reverse transcriptase-polymerase chain reaction(RT-PCR).Renal pathomorphology was observed by HE and PAS staining.Results ① Compared with normal control group,diabetic model group had the significantly increased blood sugar(P0.01)and had no significantly incresed 24 h urinary protein excretion(P0.05)at 0 w;had significantly decreased body weight(P0.01)and the significantly increased kidey weight index,serum creatinine,blood urea nitrogen,24 h urinary protein excretion,renal GLUT-1 mRNA expression(P0.01)at the end of 4th week;so did at the end of 12th week.Compared with model group,triptolide group had significantly decreased blood sugar,serum creatinine and blood urea nitrogen(P0.05),24 h urinary protein excretion and renal GLUT-1 mRNA expressions(P0.01)at the end of 8th week;and had significantly increased body weight(P0.05)and kidey weight index(P0.01)at the end of 12th week.②HE and PAS dyeing showed that glomcrulus hypertrophia,mesangial cell proliferation,mesangial matrix diffused and nodular multiplication,thicking of the glomerular and tubular basement membrane of rats inmodel group.In triptolide group these chages alleviated.Conclusions Triptolide can decrease the 24 h urinary protein excretion,inhibite the degree of renal hypertrophy and fibrosis hardening.This might be the mechanism that triptolide can down-regulate the synthesis of the expression and activity of GLUT-1 mRNA,and ultimately postpone the development of diabetic nephropathy.