摘要: AIM:To observe the effect of modified Si-Miao-San(mSMS) on advanced glycation end products(AGEs)-induced pancreatic B cell dysfunction,as well as examining the underlying mechanisms.METHOD:Pancreatic B cells(INS-1) were stimulated with advanced glycation end products(AGEs,200 gmL-1) for 24 h to produce dysfunction in pancreatic B cells and the effects of mSMS observed on insulin secretion,NF-B(p65) phosphorylation,reactive oxygen species(ROS) production,mitochondria membrane potential(m),cell apoptosis,phosphorylation of AMP-kinase(AMPK),and caspase 3 activity.RESULTS:The AGEs challenge resulted in increased basal insulin secretion,but decreased insulin secretion in response to high glucose,whereas this situation was reversed by mSMS treatment.AGEs stimulation induced NF-B(p65) phosphorylation and reactive oxygen species(ROS) production,as well as m collapse and cell apoptosis.mSMS inhibited ROS production and inhibited NF-B activation by attenuating p65 phosphorylation.Meanwhile,AGEs-induced m collapse and cell apoptosis were also reversed by mSMS treatment.Compound C,an inhibitor of AMP-Kinase(AMPK),abolished the beneficial effects of mSMS on the regulation of B cell function,indicating the involvement of AMPK.CONCLUSION:mSMS ameliorated AGEs-induced B cell dysfunction by suppressing ROS-associated inflammation,and this action was related to its beneficial regulation of AMPK activity.