Effect of dl-praeruptorin A on desmin and vimentin content in rat ischemia/reperfusion myocardiocyte

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Background Intermediate filament(IF)proteins have been thought to play a role in nuclear centration,organellemovement and maintenance of cell shape,dl-praeruptorin A(Pd-la),a novel Ca~(2+)-influx blocker and K~+-channel openerisolated from Chinese traditional herbal medicine Qian-Hu,has been demonstrated to inhibit expression of apoptosisrelated proteins and reduce the level of proinflammatory factors in ischemia/reperfusion myocardiocytes.Morphologically,whether Pd-la effects myocardiocyte IFs remains unclear.The purpose of this study was,for the first time,to evaluate thein vivo effects of Pd-la on IF desmin and vimentin content in order to further explore its cardioprotection against ischemiaand elucidate its mechanism of action.Methods Rats underwent a 30 minutes coronary occlusion followed by 120 minutes reperfusion.Assessment ofdesmin and vimentin content of myocardiocytes was performed by immunohistochemistry,Western blot,Hematoxylin-Eosin staining and densitometry.Results Pretreatment with i.v.infusion of Pd-la prior to ischemia significantly increased desmin and vimentin contentand alleviated defects caused by the ischemia/reperfusion insult,e.g.with Pd-la at a dose of 0.5 or 1.0 mg/kg,integrateddensity values of desmin were increased from 61478±10074 to 177408±10395 and 195784±20057,and vimentinfrom 59189±19853 to 164781±19543 and 185696±20957(P<0.01,vs placebo),respectively.The recovery ofdesmin seemed to be stronger and appeared earlier than that of vimentin.Conclusion Pd-la protectively increased IF desmin and vimentin content in ischemia/reperfusion myocardiocytes,which might be partially responsible for its cardioprotection against ischemia. Ca (2 +) - influx blocker and K ~ + ions have been thought to play a role in nuclear center, organellemovement and maintenance of cell shape, dl-praeruptorin A (Pd- -channel openerisolated from Chinese traditional herbal medicine Qian-Hu, has been demonstrated to inhibit expression of apoptosisrelated proteins and reduce the level of proinflammatory factors in ischemia / reperfusion myocardiocytes. Morphologically, whether Pd-la effects myocardiocyte IFs remains unclear.The purpose of this study was, for the first time, to evaluate the in vivo effects of Pd-la on IF desmin and vimentin content in order to further explore its cardioprotection against ischemia and elucidate its mechanism of action. Methods Rats underwent a 30 minutes coronary occlusion followed by 120 minutes reperfusion. Assessment of desmin and vimentin content of myocardiocytes was performed by immunohistochemistry, Western blot, Hematoxylin-Eosin staining and densitometry. Results Pretr eatment with ivinfusion of Pd-la prior to ischemia significantly increased desmin and vimentin content and alleviated defects caused by the ischemia / reperfusion insult, eg with Pd-la at a dose of 0.5 or 1.0 mg / kg, integrateddensity values ​​of desmin were increased from 61478 ± 10074 to 177408 ± 10395 and 195784 ± 20057, and vimentin from 59189 ± 19853 to 164781 ± 19543 and 185696 ± 20957 (P <0.01 vs vs placebo), respectively. The recovery ofdesminated to be stronger and sooner than that of vimentin .Conclusion Pd-la protectively increased IF desmin and vimentin content in ischemia / reperfusion myocardiocytes, which might be partially responsible for its cardioprotection against ischemia.
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