Ligustrazine regulates LPS-induced apoptosis and inflammatory response of osteoarthritis chondrocytes via inhibiting phosphorylation of NF-κB P65

Hai-Quan ZHU; Zi-Min LIU; Xiang-Sheng MENG; Xiao SUN; Li-Ming WANG

Objective:

To explore the effect of ligustrazine on the LPS-induced apoptosis and inflammatory response of osteoarthritis chondrocytes.

Methods:

Osteoarthritis model was induced by LPS. Chondrocytes were divided into four group control group, ligustrazine ( 20 μmol/L) group, LPS ( 100 ng/ml) group and ligustrazine ( 20 μmol/L) +LPS ( 100 ng/ml) group. Apoptosis was measured by Hoechst33258 staining. The levels of nitric oxide ( NO), tumor necrosis factor α ( TNF-α) and interleukin ( IL) -6 were detected by ELISA. The protein levels of collagenⅡ, aggrecan, matrix metalloproteinase 13 ( MMP-13), NF-κB P65 and p-NF-κB P65 were tested by Western blot.

Results:

The LPS-induced abnormal cell morphology and decreased number of cells were ameliorated by ligustrazine ( 20 μmol/L). The apoptosis in LPS group was higher than control group ( P＜0. 05). The LPS-induced enhancive apoptosis was reduced by ligustrazine ( P＜0. 05). Compared with control group, the expression of collagenⅡ and aggrecan was alleviated with increased expression of MMP-13 ( P＜0. 05). The LPS-induced declined expression of collagenⅡ and aggrecan and elevated expression of MMP-13 was inhibited by ligustrazine ( P＜0. 05). The levels of NO, TNF-α and IL-6 in LPS group were higher than control group ( P＜0. 05). The levels of NO, TNF-α and IL-6 in LPS+ligustrazine group were lower than LPS group ( P＜0. 05). Compared with control group, the rate of pP65/P65 in LPPS group was enhanced ( P＜ 0. 05). The LPS-indiced increased rate of p-P65/P65 was decreased by ligustrazine ( P ＜0. 05).

Conclusion:

Ligustrazine alleviates the LPS-induced apoptosis and inflammatory response of osteoarthritis chondrocytes via inhibiting phosphorylation of NF-κB P65.

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