2012年1月3日,，據(jù)《每日科學(xué)》報(bào)道，硫化氫,，一種臭名昭著的臭雞蛋氣味的氣體,，可能最終能挽回它的名譽(yù)。它可以減少腎細(xì)胞中由高糖誘導(dǎo)產(chǎn)生的蛋白質(zhì)疤痕,，得克薩斯大學(xué)健康科學(xué)中心圣安東尼奧的研究人員在《生物化學(xué)雜志》（Journal of Biological Chemistry）發(fā)表了他們的最新研究成果,。
研究論文定于2012年年初出版。
"氣體作為生物事件的調(diào)解員,，這非常的有意思,，"B.S. Kasinath說，醫(yī)學(xué)博士,、醫(yī)學(xué)教授,、圣安東尼奧醫(yī)學(xué)院腎病學(xué)家。"我們發(fā)現(xiàn),，當(dāng)我們添加硫氫化鈉到暴露于高糖的腎細(xì)胞（一種物質(zhì),，可以釋放硫化氫）中時(shí)，它減少了能致腎臟瘢痕的基質(zhì)蛋白的產(chǎn)生,。"與該結(jié)論相一致的是,，在1型或2型糖尿病小鼠內(nèi)，腎臟中促進(jìn)硫化氫產(chǎn)生的酶減少了,， Kasinath博士和他的團(tuán)隊(duì)報(bào)道稱,。
腎臟中的瘢痕，稱之為腎纖維化,，是導(dǎo)致終末期腎病的核心缺陷,。在美國近一半終末期腎臟病與糖尿病有關(guān),，糖尿病是血糖調(diào)節(jié)能力較弱為標(biāo)志的一種疾病。
"我們已經(jīng)找到一種方法能夠減少基質(zhì)蛋白的合成,，這是糖尿病中一個(gè)很重要的問題,，"Kasinath博士說。"因?yàn)檫@些研究僅局限于細(xì)胞,，研究結(jié)果不宜被擴(kuò)展外推到人類糖尿病腎病的治療,，他強(qiáng)調(diào)道。
這一發(fā)現(xiàn)為研究老鼠或其他動物模型鋪平了道路,。硫化氫的安全性和有效性都應(yīng)該在腎臟疾病動物模型中進(jìn)行測試,，之后才能考慮人體試驗(yàn)。這種防范措施是必要的,，因?yàn)榱蚧瘹湓谳^高濃度時(shí),，是一種有毒物質(zhì)。
生物化學(xué)編輯將該團(tuán)隊(duì)的稿件選為每周論文,，設(shè)為所有稿件中占1％的極具意義和重要性的研究稿件,。生物化學(xué)期刊每年發(fā)表超過6600篇論文，其中大約只有50~100篇能夠獲此殊榮,。
Hak Joo Lee博士,，腎臟病科的博士后研究人員，是該研究的第一作者,。 Kasinath博士,，Barshop長壽和老年化健康科學(xué)中心的成員，是研究的通訊作者,，表達(dá)了對該項(xiàng)研究的其他共同作者的貢獻(xiàn)表示肯定,。
這項(xiàng)工作由國家衛(wèi)生研究院/國家糖尿病、消化道和腎臟疾病研究所（DK077295）以及一個(gè)美國退伍軍人事務(wù)部授予首席研究員Kasinath博士的研究資助,。（生物谷bioon.com）
doi:10.1074/jbc.M111.278325
PMC:
PMID:
Hydrogen sulfide inhibits high glucose-induced matrix protein synthesis by activating AMP-activated protein kinase in renal epithelial cells
H. J. Lee, M. M. Mariappan, D. Feliers, R. C. Cavaglieri, K. Sataranatarajan, H. E. Abboud, G. Ghosh Choudhury, B. S. Kasinath.
Capsule: Background: If hydrogen sulfide regulates protein synthesis is not known. Results: In kidney cells, hydrogen sulfide inhibited high glucose-induced synthesis of proteins including matrix proteins by activating AMP-activated protein kinase and inhibiting events in mRNA translation. Conclusion: Hydrogen sulfide reduces high glucose stimulation of matrix protein synthesis in renal cells. Significance: Hydrogen sulfide induction may inhibit kidney matrix protein accumulation in diabetes. Abstract: Hydrogen sulfide, a signaling gas, affects several cell functions. We hypothesized that hydrogen sulfide modulates high glucose (HG, 30 mM) stimulation of ma-trix protein synthesis in glomerular epithelial cells (GECs). HG stimulation of global protein synthesis, cel-lular hypertrophy, and matrix laminin and type IV col-lagen content was inhibited by NaHS, a H2S donor. HG activation of mTOR complex1 (mTORC1), shown by phosphorylation of p70S6 kinase and 4E-BP1, was in-hibited by NaHS. HG recruited mTORC1 to promote key events in the initiation and elongation phases of mRNA translation: binding of eIF4A to eIF4G, reduc-tion in PDCD4 expression and inhibition of its binding to eIF4A, eEF2 kinase phosphorylation and dephos-phorylation of eEF2; these events were inhibited by NaHS. Role of AMPK, an inhibitor of protein synthesis, was examined. NaHS dose-dependently stimulated AMPK phosphorylation and restored AMPK phos-phorylation reduced by HG. Compound C, an AMPK inhibitor, abolished NaHS effect on events in mRNA translation as well as global and matrix protein synthe-sis. NaHS induction of AMPK phosphorylation was in-hibited by siRNA for Ca calmodulin kinase kinase beta (CaMKKbeta), but not LKB1, upstream kinases for AMPK; STO-609, a CaMKKbeta inhibitor, had the same effect. Renal cortical content of cystathionine beta synthase and cystathionine gamma lyase, hydrogen sulfide generating enzymes, was significantly reduced in mice with type 1 diabetes or type 2 diabetes, coinciding with renal hyper-trophy and matrix accumulation. Hydrogen sulfide is a newly identified modulator of protein synthesis in the kidney and reduction in its generation may contribute to kidney injury in diabetes.
