{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,2]],"date-time":"2026-06-02T01:20:43Z","timestamp":1780363243648,"version":"3.54.1"},"reference-count":48,"publisher":"S. Karger AG","issue":"2","license":[{"start":{"date-parts":[[2017,1,1]],"date-time":"2017-01-01T00:00:00Z","timestamp":1483228800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"},{"start":{"date-parts":[[2017,1,1]],"date-time":"2017-01-01T00:00:00Z","timestamp":1483228800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Kidney Blood Press Res"],"published-print":{"date-parts":[[2017]]},"abstract":"<jats:p>&lt;b&gt;&lt;i&gt;Background\/Aims:&lt;\/i&gt;&lt;\/b&gt; Chelerythrine (CHE), a benzophenanthridine alkaloid, is a potent, selective, and cell-permeable protein kinase C (PKC) inhibitor. The purpose of the present study was to evaluate the effect of CHE on myocardial recovery after renal ischemia\/reperfusion (I\/R)-induced myocardial injury (RI\/RMI) in a streptozocin (STZ)-induced diabetic rat model. &lt;b&gt;&lt;i&gt;Methods:&lt;\/i&gt;&lt;\/b&gt; Diabetes mellitus (DM) rats preconditioned with CHE and D, L-propargylglycine (PAG) were subjected to renal I\/R. The extent of cardiac morphologic lesions and the biochemical markers of cardiorenal function and oxidative stress were detected utilizing hematoxylin-eosin staining, commercial kits, and enzyme-linked immunoassay, respectively. The expressions of cystathionine-\u03b3-lyase (CSE), PKC-\u03b1, PKC-\u03b2&lt;sub&gt;2&lt;\/sub&gt;, and nuclear factor-kappa B (NF-\u03baB) in the rat myocardial tissue were measured utilizing western blotting. &lt;b&gt;&lt;i&gt;Results:&lt;\/i&gt;&lt;\/b&gt; Renal I\/R treatment resulted in myocardial injury. CHE-preconditioning promoted the recovery from myocardial damage by ameliorating the biochemical parameters of myocardial injury, reducing oxidative stress, increasing the H&lt;sub&gt;2&lt;\/sub&gt;S level, up-regulating the expression of CSE, and down-regulating the expressions of PKC-\u03b1, PKC-\u03b2&lt;sub&gt;2&lt;\/sub&gt;, and NF-\u03baB. &lt;b&gt;&lt;i&gt;Conclusion:&lt;\/i&gt;&lt;\/b&gt; These findings suggest that CHE-pretreatment may exert a protective effect on the myocardium against RI\/RMI by activating endogenous CSE\/H&lt;sub&gt;2&lt;\/sub&gt;S via PKC\/NF-\u03baB pathway in STZ-induced diabetic rats. Further studies are needed defining underlying mechanisms.<\/jats:p>","DOI":"10.1159\/000477948","type":"journal-article","created":{"date-parts":[[2017,6,16]],"date-time":"2017-06-16T21:03:01Z","timestamp":1497646981000},"page":"379-388","source":"Crossref","is-referenced-by-count":32,"title":["Chelerythrine Attenuates Renal Ischemia\/\nReperfusion-induced Myocardial Injury by\nActivating CSE\/H2S via PKC\/NF-\u03baB Pathway in Diabetic 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