Impact of Salidroside on Mitochondrial Fission in Vascular Smooth Muscle Cell s under High Glucose Conditions and Its Possible Mechanism

Zhuang Xinyu; Gao Xiufang; Shi Haiming

doi:10.3969/j.issn.1672-1349.2017.01.008

Abstract：Objective To investigate the impact of salidroside on vascular smooth muscle cells (VSMCs)proliferation and mitochon-drial dynamics under high glucose conditions,and its possible mechanism.Methods The VSMCs in proliferative phase were random-ly divided into two groups:low glucose group cultured low glucose (5 mmol/L),and high glucose group cultured high glucose (25 mmol/L).Then VSMCs in each group were divided into five subgroups:control group,low concentration salidroside group (0.3 mmol/L), high concentration salidroside group (0.5 mmol/L),low concentration Mdivi-1 group (10μmol/L),high concentration Mdivi-1 group (25μmol/L).VSMCs were cultured by low or high concentration of salidroside or Mdivi-1 under high glucose or low glucose condition for 24 hours.The expressions of proteins related to mitochondrial dynamics including dynamin-related protein (Drp1)and mitofusin 2 (Mfn2)were tested by western blot and real-time polymerase chain reaction (PCR).The mitochondria inner membrane was ob-served under laser scanning confocal microscope (LSCM).The mitochondrial fission count (MFC)was analyzed by Image J soft-ware.Then Mfn2 was inhibited by smal interfering RNA (siRNA).VSMCs proliferation was observed.Results VSMCs was abnormal y proliferated,mitochondrial fission increased,Drp1 expression increased,and Mfn2 expression reduced under high glucose condition. Salidroside and an inhibitor of Drp1 (Mdivi-1)can inhibit VSMCs proliferation,Drp1 expression and mitochondrial fission and up regulate Mfn2 expression (all P<0.05).After using siRNA to silence Mfn2 expression,the inhibitive effect on VSMCs proliferation can be partly reversed.Conclusion Salidroside can inhibit VSMCs proliferation induced by-high glucose and may act its therapeutic effect via inhibiting mitochondrial fission by down regulation of Drp1 expression and up-regulation of Mfn2 expression.