SF induced Trx in murine retina and effectively reduced retinal light damage. Evidence suggests that the ARE is involved in the mechanism of Trx induction by SF in RPE cells.

We have cloned the gene of a new transmembrane-type serine protease from rat kidney, which activates sodium channels. The amino acid sequence deduced from a full-length cDNA revealed that transmembrane serine protease-1 (TMSP-1) is a member of the clan SA/family S1 of serine proteases, comprising a 30 amino acid prepropeptide, a mature form sequence of 274 amino acids starting with the Ile-Val-Gly-Gly-Gln motif, and a common catalytic triad of serine proteases. The hydrophobic amino acid sequence in the carboxy-terminus of this enzyme suggests that it is a glycosylphosphatidylinositol-anchored protein. As revealed by quantitative reverse transcription-polymerase chain reaction analysis, it is highly expressed in kidney, small intestine, and stomach, and moderately expressed in lung, thymus, spleen and skin. The recombinant protease had an optimal pH at 9.0, selectively cleaved synthetic peptide substrates of trypsin, and was inhibited by aprotinin, leupeptin and benzamidine. Immunohistochemical studies revealed that this protease is predominantly expressed in cells from collecting ducts of the renal medulla. We also demonstrate that a C-terminally truncated variant of TMSP-1 significantly activates the epithelial sodium channel, and that its mRNA levels are upregulated by aldosterone. These observations suggest that it is a new member of the trypsin-type transmembrane proteases, which regulate sodium balance by activating the epithelial sodium channel.

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AimHigh alcohol consumption leads to alcohol‐related disease. The aim of this study was to explore the effects of Sasa veitchii extract (SE) on ethanol‐induced liver injury.MethodsOf four groups of 7‐week‐old male mice (control, SE, ethanol, and SE + ethanol groups), SE and SE + ethanol groups were orally treated with SE once a day for 3 days. Twenty‐four hours after the last administration, the SE + ethanol and ethanol groups were intraperitoneally injected with ethanol (2 g/kg). The mice in each group were euthanized 24 h after ethanol administration, and blood and livers were collected.ResultsHistopathological examination of the livers of ethanol‐treated mice revealed a depletion of glycogen. Ethanol injection resulted in high plasma levels of alanine aminotransferase and aspartate aminotransferase and high levels of hepatic lipid peroxidation and inflammatory cytokines. Pretreatment with SE reversed all these changes in SE + ethanol mice compared to that in the ethanol group. Moreover, SE injection increased the hepatic protein levels of aldehyde dehydrogenase 2.ConclusionOur results show that SE protected the mice against acute ethanol‐induced hepatic injury by modulating oxidative stress and ethanol metabolism, and hence, could be explored for treatment of alcohol‐related disease.

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