Roles of tricin in eliminating LPS-induced inflammatory response in HUVECs
[Objective]This study aimed to evaluate the protective effect of tricin on inflammatory in-jury in human umbilical vein endothelial cells(HUVECs)induced by lipopolysaccharide(LPS).[Method]HUVECs were used as the research subject.The MTT method was employed to determine the optimal con-centration of tricin for treatment.ELISA was utilized to determine the appropriate LPS concentration for modeling and to assess the expression of inflammation-related factors(TNF-α,iNOS,COX-2,IL-1,IL-6)in HUVECs.Western blot analysis was performed to detect the protein expression of NF-κB and MAPK signal pathways(β-Actin,P65,IKB,P-P65,P-IKB,P38,JNK,ERK1/2,P-P38,P-JNK,P-ERK1/2).[Result]Different concentrations of LPS were found to promote the expression of TNF-α(P<0.01),with the highest expression observed at LPS concentrations between 2.5 μg/mL and 7.5 μg/mL.Therefore,2.5 μg/mL was chosen as the modeling concentration.At this concentration,LPS induced the upregulation of inflammation-related factors and pathway proteins(P<0.01),while simvastatin,used as the positive con-trol,inhibited the expression of these factors and proteins induced by LPS(P<0.01).HUVECs exhibited no significant difference in activity within tricin concentrations up to 3 μg/ml;therefore,tricin high(3 μg/mL),medium(2 μg/mL),and low(1 μg/mL)dosage groups were selected.Tricin in these dosage groups effec-tively downregulated the expression of inflammation-related factors and pathway proteins induced by LPS(P<0.01).Tricin showed a weaker inhibitory effect on inflammation-related factors compared to simvas-tatin,while its inhibitory effect on inflammation-related pathway proteins was stronger than that of simvas-tatin.The expression of inflammation-related factors decreased with increasing tricin concentration(P<0.01),and a similar downward trend was observed for inflammation-related pathway proteins.[Conclusion]The findings indicated that tricin can attenuate LPS-induced inflammatory damage in HU-VECs by inhibiting the NF-κB and MAPK signaling pathways.
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