摘要
Background Intermediate filament （IF） proteins have been thought to play a role in nuclear centration, organelle movement and maintenance of cell shape, dl-praeruptorin A （Pd-la）, a novel Ca^2＋-influx blocker and K^＋-channel opener isolated from Chinese traditional herbal medicine Qian-Hu, has been demonstrated to inhibit expression of apoptosis related 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 Pretreatment with i.v. infusion of Pd-la prior to ischemia significantly increased desmin and vimentin content and alleviated defects caused by the ischemia/reperfusion insult, e.g. with Pd-la at a dose of 0.5 or 1.0 mg/kg, integrated density values of desmin were increased from 61 478 ± 10 074 to 177 408 ±10 395 and 195 784±20 057, and vimentin from 59 189± 19 853 to 164 781± 19 543 and 185 696± 20 957 （P〈0.01, vs placebo）, respectively. The recovery of desmin 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.
Background Intermediate filament （IF） proteins have been thought to play a role in nuclear centration, organelle movement and maintenance of cell shape, dl-praeruptorin A （Pd-la）, a novel Ca^2＋-influx blocker and K^＋-channel opener isolated from Chinese traditional herbal medicine Qian-Hu, has been demonstrated to inhibit expression of apoptosis related 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 Pretreatment with i.v. infusion of Pd-la prior to ischemia significantly increased desmin and vimentin content and alleviated defects caused by the ischemia/reperfusion insult, e.g. with Pd-la at a dose of 0.5 or 1.0 mg/kg, integrated density values of desmin were increased from 61 478 ± 10 074 to 177 408 ±10 395 and 195 784±20 057, and vimentin from 59 189± 19 853 to 164 781± 19 543 and 185 696± 20 957 （P〈0.01, vs placebo）, respectively. The recovery of desmin 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.
基金
This study was partly supported by a grant from the Key Foundation of Ministry of Public Health of China(No.88402257)
