CAJ | 학술논문

目的：研究川穹嗪（ TMP）对阿霉素诱导的急性心衰（ AHF）小鼠心肌损伤和凋亡的保护作用及机制。方法动物分为对照组（10 mL · kg-1· d-10.9％NaCl）、模型组（阿霉素20 mg· kg-1· d-1，连续2次）、依那普利组（10 mg· kg-1· d-1）和高、中、低3个剂量（60，30，15 mg· kg-1· d-1） TMP组，连续给药2周后，阿霉素诱导建立AHF模型，检测心肌酶谷草转氨酶（ AST ）、肌酸激酶（ CK）及肌酸激酶同工酶（ CK-MB）水平的变化。苏木精-伊红（ HE）染色进行病理学检查，Western-Blot检测心肌Bax和Bcl-2的表达变化。结果模型组血清心肌酶的水平升高，心肌受损并且有炎症浸润，TMP组和依那普利组的心肌酶的水平显著降低，心肌损伤及炎症得到明显改善。 TMP和依那普利可以降低AHF小鼠心肌bax表达而增加Bcl-2的表达。结论 TMP对阿霉素诱导的AHF小鼠心肌具有保护作用，其机制可能与TMP防止心肌细胞损伤和凋亡有关。
목적：연구천궁진（ TMP）대아매소유도적급성심쇠（ AHF）소서심기손상화조망적보호작용급궤제。방법동물분위대조조（10 mL · kg-1· d-10.9％NaCl）、모형조（아매소20 mg· kg-1· d-1，련속2차）、의나보리조（10 mg· kg-1· d-1）화고、중、저3개제량（60，30，15 mg· kg-1· d-1） TMP조，련속급약2주후，아매소유도건립AHF모형，검측심기매곡초전안매（ AST ）、기산격매（ CK）급기산격매동공매（ CK-MB）수평적변화。소목정-이홍（ HE）염색진행병이학검사，Western-Blot검측심기Bax화Bcl-2적표체변화。결과모형조혈청심기매적수평승고，심기수손병차유염증침윤，TMP조화의나보리조적심기매적수평현저강저，심기손상급염증득도명현개선。 TMP화의나보리가이강저AHF소서심기bax표체이증가Bcl-2적표체。결론 TMP대아매소유도적AHF소서심기구유보호작용，기궤제가능여TMP방지심기세포손상화조망유관。
Objective To investigate the protective effect of tetramethyl-prazine ( TMP ) on adriamycin ( ADR ) -induced acute heart failure ( AHF) and underlying molecular mechanisms.Methods Male Kun-ming mice were randomly divided into six groups: control group (0.9%NaCl 10 mL· kg -1· d-1), model group (ADR 20 mg· kg -1, continuous twice ) , enalapril group ( 10 mg · kg -1 · d-1 ) and TMP high, middle and low dose groups (60, 30, 15 mg· kg-1 · d -1 ).All groups were administered drugs for 2 weeks, then ADR 20 mg· kg -1 was given intraperitoneally twice to establish AHF model.Cardiac enzymes including aspartate aminotransferase (AST), creatine kinase (CK) and MB isoenzyme of creatine kinase ( CK-MB) were detected.Histopatho-logical examination was performed by hematoxylin -eosin ( HE ) stai-ning.Western-blot analysis was used to investigate the expression levels of Bax and Bcl-2.Results AST, CK and CK-MB of left ventricle of AHF mice showed a significant increase while TMP treatment decreased their levels in myocardial tissue.Myocardial tissue of AHF mice was damaged and myocardial fiber arranged disorderly.Myocardial cells showed vacuolar degeneration and necrosis in AHF mice.Administration of TMP obviously attenuated myocardial damage and myocardial fiber disordered arrangement.Further studies revealed that TMP decreased the expression of pro -apoptotic factor of Bax and pro-inflammatory cytokine TNF-αwhile increased the expression of anti -apoptotic factor of Bcl-2.Conclusion TMP exerts protective effect on adriamycin -induced AHF partially by inhibition of cardiomyocytes apoptosis and cardi-ac enzymes levels .