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Lactic acid inhibits lipopolysaccharide-induced translocation of NF-κB p65 from cytoplasm to nucleus and transcription of nuclear factor-κB p65 and cyclooxygenase 2
JIANG Jin-qi XU Guang-yong SHI Ya-ran QIAO Yu HU Ge1 REN Xiao-min*
Acta Anatomica Sinica ›› 2013, Vol. 44 ›› Issue (2) : 204-209.
Lactic acid inhibits lipopolysaccharide-induced translocation of NF-κB p65 from cytoplasm to nucleus and transcription of nuclear factor-κB p65 and cyclooxygenase 2
Objective To investigate whether lactic acid(LA),which was extracted from the culture supernatant of Lactobacillus,could inhibit lipopolysaccharide(LPS)-induced translocation of NF-κB p65 from cytoplasm to nucleus and transcription of NF-κB p65 and cyclooxygenase 2(COX-2). Methods Rat intestinal mucosa microvascular endothelial cells(RIMMVEs) were cultured in vitro and were divided into 4 groups:control group,LPS group,LA pretreated group and NF-κB inhibitor (pyrrolidinecarbodithioate,PDTC) pretreated group.The protein of NF-κB p65 in cytoplasm and in nucleus was detected by Western blotting analysis after RIMMVEs were treated with LPS for 30 minutes.The mRNA of NF-κB p65 and COX-2 was detected by real time quantity-PCR after RIMMVEs were treated with LPS for 9 hours. Results In a short time(treated with LPS for 30 minutes),the protein expression of NF-κB p65 had no notable difference but the ratios of p65 in nuclei of LA and PDTC pretreated group were notably lower than that of LPS group.After a longer time(treated with LPS for 9 hours),the mRNA expression of NF-κB p65 and COX-2 were notably lower than LPS group. Conclusion LA has the effects like NF-κB inhibitor,notably inhibiting LPS-induced translocation of NF-κB p65 from cytoplasm to nucleus and transcription of NF-κB p65 and COX-2.By this way,LA inhibits inflammatory response.
Lactic acid / Lipopolysaccharide / Nuclear factor-κB / Cyclooxygenase 2 / Mucosa microvascular endothelial cells / Western blotting / Real time quantity-PCR / Rat
[1] Kumar A, Takada Y, Boriek AM, et al. Nuclear factor-kappa B: its role in health and disease [J]. J Mol Med,2004,82(7):434-448.
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