OBJECTIVETo study the distribution of IS605, IS606 among clinical isolates of Helicobacter pylori in China.

METHODSA total of 104 H.pylori strains isolated from 5 different geographic regions in China were analyzed by PCR and dot-blot.

RESULTSForty-two strains out of the 104 isolates from 5 regions in China were found containing IS605 with 19 containing IS606. The frequency (66%) of IS605 positive strains from Yunnan province was higher than that from other areas. The different distribution of IS606 was neither associated with geographical regions nor with the presence of IS605 but IS606 were associated with the different clinical outcomes. However, the two reading frames ORFA and ORFB of IS605 were constantly coexisting.

CONCLUSIONIn China, IS605 and IS606 of H. pylori were widely existing but the presence of IS605 in H. pylori might be associated with geographic origin.

DNA Transposable Elements ; Helicobacter pylori ; genetics ; Humans ; Polymerase Chain Reaction

Evidence indicates that metabolic reprogramming characterized by the changes in cellular metabolic patterns contributes to the pathogenesis of pulmonary fibrosis(PF).It is considered as a promising ther-apeutic target anti-PF.The well-documented against PF properties of Tanshinone ⅡA(Tan ⅡA)have been primarily attributed to its antioxidant and anti-inflammatory potency.Emerging evidence suggests that TanⅡA may target energy metabolism pathways,including glycolysis and tricarboxylic acid(TCA)cycle.However,the detailed and advanced mechanisms underlying the anti-PF activities remain obscure.In this study,we applied[U-13C]-glucose metabolic flux analysis(MFA)to examine metabolism flux disruption and modulation nodes of Tan ⅡA in PF.We identified that Tan ⅡA inhibited the glycolysis and TCA flux,thereby suppressing the production of transforming growth factor-β1(TGF-β1)-dependent extracellular matrix and the differentiation and proliferation of myofibroblasts in vitro.We further revealed that Tan ⅡA inhibited the expression of key metabolic enzyme hexokinase 2(HK2)by inhibiting phosphoinositide 3-kinase(PI3K)/protein kinase B(Akt)/mammalian target of rapamycin(mTOR)/hypoxia-inducible factor 1α(HIF-1α)pathway activities,which decreased the accumulation of abnormal metabolites.Notably,we demonstrated that Tan ⅡA inhibited ATP citrate lyase(ACLY)activity,which reduced the collagen synthesis pathway caused by cytosol citrate consumption.Further,these results were validated in a mouse model of bleomycin-induced PF.This study was novel in exploring the mechanism of the occurrence and develop-ment of Tan ⅡA in treating PF using 13C-MFA technology.It provided a novel understanding of the mechanism of Tan ⅡA against PF from the perspective of metabolic reprogramming.