Abstract: Ｏｂｊｅｃｔｉｖｅ：To investigate effect of 1,25(OH)2D3 on hyperglycosisinduced podocyte injury and its mechanism.
Ｍｅｔｈｏｄｏｌｏｇｙ：MPC5 cells were divided into six groups:normal glucose concentration group(NG),high glucose group(HG),Mannitol osmotic pressure control(NG+M)，high glucose + 1,25(OH)2D3 intervention group(HG+VD),high glucose + 1,25(OH)2D3+ 3methyladenine intervention group(HG+VD+3MA),high glucose+1,25(OH)2D3+PI3K inhibitor LY294002 group(HG+VD+ LY294002)Cell viability was analyzed by CCK8 methodBy immunofluorescence technique to observe autophagy related protein expression of LC3Ⅱ;Western blotting was used to detect the expression of autophagyrelated proteins Beclin1,P62,pathway related proteins PI3K,Akt,antiapoptotic proteins Bcl2 and apoptotic proteins Bax and caspase3.
Ｒｅｓｕｌｔｓ：1High glucose can induce apoptosis of podocytes,and active vitamin D3 can reduce the apoptosis of podocytes induced by high glucose.2Active vitamin D3 can reverse the downregulation of autophagy in highglycosylated podocytes,and autophagy inhibitor 3methyladenine(3MA) can block the protective effect of active vitamin D on highglycosylated podocytes.3Active vitamin D3 activates PI3K/Akt signal,and LY294002 blocks the protective effect on podocytes and upregulates autophagy.
Ｃｏｎｃｌｕｓｉｏｎ：
Active vitamin D3 can regulate autophagy through  PI3K/Akt signaling pathway to alleviate highglycoseinduced podocyte injury and apoptosis.

Key words: 1, 25(OH)2D3, autophagy, apoptosis, podocyte, PI3K/Akt signaling pathway