Inhibitory effect of metformin on inflammatory response of kupffer cells of liver in diabetic mice and its improvement on phagocytic function / 吉林大学学报(医学版)

ABSTRACT

Objective: To observe the inhibitory effect of metformin on the inflammatory response of Kupffer cells (KCs) of liver in the diabetic mice, and to explore its improvement on the phagocytic function of KCs. and to elucidate the protective mechanism of metformin on the KCs in the diabetic mice. Methods: The C57BLKS/J db/db mice were divided into diabetes group and diabetes metformin group, and die C57BLKS/J db/m mice were divided into non-diabctcs group and non-diabctcs + metformin group. 8 micc in cach group. The KCs were culturcd in vitro and the changcs of ultrastrusturcs of KCs were observed by transmission electron microscope. The levels of intcrleukin 6 (1L-6), tumor necrosis factor a (TNF-a) and y-intcrfcron (INF-7) in the KCs were detected by EL1SA. The expression levels of intercellular adhesion molecule 1 (ICAM-1) protein in the KCs was detected by Western blotting method. Transwcll chamber assay was used to detect the neutrophil chemotaxis ability of the KCs. and the phagocytic ability of KCs was observed under inverted microscope. Results: The number of mitochondria and rough endoplasmic reticulum (RER) in the KCs of the diabetic micc was reduced, the RER expanded, the mitochondria swelled, and die lipid droplets were increased. Compared with non-diabctcs group, the levels of 1L-6 , TNF-a. INF-y and the expression level of ICAM-1 in die KCs of the micc in diabetes group were significantly increased ( P<0. 05)s the neutrophil chemotaxis ability of the KCs was enhanced ( P<0. 05). and the phagocytic ability was decreased ( P< 0. 05). Compared with diabetes group, the levels of 1L-6, TNF-a, INF-y and the expression level of ICAM-1 in the KCs in diabetes + metformin group were significandy decreased ( P<0. 05)s the neutrophil chemotaxis ability was decreased ( P∗. 0. 05), and the phagocytic ability was enhanced ( P∗C0.05). Conclusion: Metformin can inhibit the inflammatory response of KCs in the diabetic mice and improve its phagocytic function and protect the KCs.