Chlorogenic acid regulates lipopolysaccharide-induced apoptosis and inflammatory response of human retinal vascular endothelial cells / 中国免疫学杂志

ABSTRACT

Objective: Diabetic retinopathy is one of the most common complications of diabetes. This study aims to explore the effect of chlorogenic acid ( CA) on lipopolysaccharide ( LPS) -induced apoptosis and inflammatory response of human retinal vascular endothelial cells ( HRECs). Methods: Cell proliferation was tested by CCK-8. Cell apoptosis was detected by flow cytometry. The levels of IL-6, TNF-α and IL-10 were measured by ELISA. The protein levels of Ki67, Bcl-2, Caspase-3, Bax, NF-κB P65 and P-NF-κB P65 were detected by Western blot. Results: The low concentration ( ＜50 μmol/L) of CA had no effect on cell viability of HRECs. The cell viability of HRECs was decreased by high concentration (＞ 50 μmol/L) of CA. Compared with control group, the proliferation in LPS group was reduced with enhancive apoptosis ( P ＜ 0. 05). Compared with LPS group, the proliferation in CA ( 20, 50 μmol/L) group was increased with attenuated apoptosis ( P ＜ 0. 05). The protein levels of Ki67 and Bcl-2 in LPS group were lower than control group ( P ＜0. 05). And the expression of Caspase-3 and Bax in LPS group was higher than control group ( P＜0. 05). Compared with LPS group, the protein levels of Ki67 and Bcl-2 in CA ( 20, 50 μmol/L) group were elevated with decreased expression of Caspase-3 and Bax ( P ＜0. 05). Moreover, the levels of IL-6 and TNF-α in LPS group were higher than control group ( P＜0. 05). And the levels of IL-10 in LPS group were lower than control group ( P＜0. 05). Compared with LPS group, the levels of IL-6 and TNF-α in CA ( 20, 50 μmol/L) group were reduced with enhanced levels of IL-10 ( P＜0. 05). In addition, the rate of p-P65/P65 in LPS group was higher than control group ( P＜0. 05). The rate of p-P65/P65 in CA ( 10, 20, 50 μmol/L) group was lower than LPS group ( P＜0. 05). Conclusion: Chlorogenic acid alleviates LPS-induced enhancive apoptosis and inflammatory response of HRECs via inhibiting activation of NF-κB P65.