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The protection mechanism of hydrogen sulfide (H<jats:sub>2<\/jats:sub>S) and the specific role of conventional protein kinase C \u03b2II (cPKC\u03b2II)\/Akt signaling pathway in the formation of atherosclerosis is still controversial.<\/jats:p>\n              <\/jats:sec>\n              <jats:sec>\n                <jats:title>Methods<\/jats:title>\n                <jats:p>8-week-old male ApoE<jats:sup>\u2212\/\u2212<\/jats:sup> mice were treated with 5\/6 nephrectomy and high-fat diet to make uremia accelerated atherosclerosis (UAAS) model. Mice were divided into normal control group (control group), sham operation group (sham group), UAAS group, L-cysteine group (UAAS+L-cys group), sodium hydrosulfide group (UAAS+NaHS group), and propargylglycine group (UAAS+PPG group). Western blot was used to detect cPKC\u03b2II activation, Akt phosphorylation and endothelial nitric oxide synthase (eNOS) expression in mice aorta.<\/jats:p>\n              <\/jats:sec>\n              <jats:sec>\n                <jats:title>Results<\/jats:title>\n                <jats:p>The membrane translocation of cPKC\u03b2II in UAAS group was higher than sham group, and L-cys or NaHS injection could suppress the membrane translocation, but PPG treatment resulted in more membrane translocation of cPKC\u03b2II (<jats:italic>P<\/jats:italic>\u2009&lt;\u20090.05, <jats:italic>n<\/jats:italic>\u2009=\u20096 per group). Akt phosphorylation and the eNOS expression in UAAS group was lower than sham group, and L-cys or NaHS injection could suppress the degradation of Akt phosphorylation and the eNOS expression, but PPG treatment resulted in more decrease in the Akt phosphorylation and the eNOS expression (<jats:italic>P<\/jats:italic>\u2009&lt;\u20090.05, <jats:italic>n<\/jats:italic>\u2009=\u20096 per group).<\/jats:p>\n              <\/jats:sec>\n              <jats:sec>\n                <jats:title>Conclusion<\/jats:title>\n                <jats:p>Endogenous cystathionine-\u03b3-lyase (CSE)\/H<jats:sub>2<\/jats:sub>S system protected against the formation of UAAS via cPKC\u03b2II\/Akt signal pathway. The imbalance of CSE\/H<jats:sub>2<\/jats:sub>S system may participate in the formation of UAAS by affecting the expression of downstream molecule eNOS, which may be mediated by cPKC\u03b2II\/Akt signaling pathway.<\/jats:p>\n              <\/jats:sec>","DOI":"10.1186\/s12882-019-1550-4","type":"journal-article","created":{"date-parts":[[2019,9,14]],"date-time":"2019-09-14T05:02:37Z","timestamp":1568437357000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":12,"title":["Molecular mechanisms of hydrogen sulfide against uremic accelerated atherosclerosis through cPKC\u03b2II\/Akt signal pathway"],"prefix":"10.1186","volume":"20","author":[{"given":"Ruifang","family":"Xiong","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xiangxue","family":"Lu","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jinghong","family":"Song","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2869-6911","authenticated-orcid":false,"given":"Han","family":"Li","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shixiang","family":"Wang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2019,9,14]]},"reference":[{"key":"1550_CR1","doi-asserted-by":"publisher","first-page":"154","DOI":"10.1016\/j.ejphar.2017.03.053","volume":"816","author":"C Christoffersen","year":"2017","unstructured":"Christoffersen C, Bartels ED, Aarup A, Nielsen LB, Pedersen TX. 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