Objective: To investigate the effects of penehyclidine hydrochloride (PHC) on lipopolysaccharide (LPS)-induced inflammatory injury of airway smooth muscle cells(AMSC) and P38MAPK/JNK pathway.Methods: HumanASMCwere cultured in vitro. ASMCwere randomly divided into 5 groups:control group (only ASMC cells were included), LPS group(the final concentration of the above cells was 500 ng·ml-1 LPS), 1, 10, 100 μmol·L-1 PHC+LPS group(the final concentration of 1, 10, 100 μmol·L-1 PHC was added on the basis of LPS group). The proliferation of ASMC was detected using CCK-8 method; the changes of cell morphology were observed under microscope; LDH and MDA levels of ASMC were detected by enzyme-linked immunosorbent assay (ELISA); Annexin V/PI double staining was used to detect apoptosis; Western blotting was used to detect apoptosis and P38MAPK/JNK pathway related protein expression. Results: Compared with the control group, the absorbance(A)value at 48 h of LPS group decreased significantly (P<0.05), ASMCwere small and flat, round in shape, empty and bright in cytoplasm, the levels of LDH and MDA were significantly increased (P<0.05), the apoptosis rate increased significantly (P<0.05), the expression level of Bcl-2 decreased significantly (P<0.05), the expression level of Bax was significantly increased (P<0.05), and the expression levels of p-JNK and p-P38 were significantly increased (P<0.05); After treatment of penehyclidine hydrochloride, compared with LPS group, the A value at 48 h of cells in 1,10,100 μmol·L-1 ICA+LPS group increased significantly (P<0.05), there was no obviously morphological change, and the number of adherent cells was more than that in LPS group, the levels of LDH and MDA decreased significantly (P<0.05), the apoptotic rate decreased significantly (P<0.05), the expression level of Bcl-2 was significantly increased (P<0.05), the expression level of Bax protein decreased significantly (P<0.05), the expression levels of p-JNK and p-P38 decreased significantly (P<0.05),which showed a dose-dependent manner. Conclusion: PHC can inhibit the inflammatory injury of ASMC induced by LPS, and the mechanism may be related to the inhibition of P38MAPK/JNK pathway activation.
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