CAJ | 학술논문

目的：研究穿心莲内酯（AP）对小鼠急性四氯化碳（CCl4）肝损伤的保护作用及其机制。方法：40只小鼠随机分成5组，正常对照组、肝损伤模型组、AP低剂量组（50 mg/kg）、高剂量组（100 mg/kg）和阳性药物组。分别测定小鼠血清中丙氨酸氨基转移酶（ALT）、天门冬氨酸氨基转移酶（AST）含量；肝匀浆中丙二醛（MDA）、还原型谷胱甘肽（GSH）的含量及肝组织病理学变化；逆转录PCR（RT-PCR）检测小鼠肝脏中肿瘤坏死因子α（TNF-α）、血红素加氧酶-1（HO-1）mRNA水平。结果：AP高剂量组（100 mg/kg）降低小鼠血清中ALT、AST水平，提高肝组织中GSH活性，降低MDA水平，差异均有统计学意义（P＜0．05）；病理镜检显示AP高剂量组明显减轻肝损伤；RT-PCR结果显示，AP高剂量组TNF-α表达水平降低，而HO-1表达增强，差异均有统计学意义（P＜0．05）。结论：AP通过抑制脂质过氧化反应，降低组织中氧自由基的生成保护急性四氯化碳肝损伤，其机制可能与抑制TNF-α的表达，诱导HO-1表达有关。
목적：연구천심련내지（AP）대소서급성사록화탄（CCl4）간손상적보호작용급기궤제。방법：40지소서수궤분성5조，정상대조조、간손상모형조、AP저제량조（50 mg/kg）、고제량조（100 mg/kg）화양성약물조。분별측정소서혈청중병안산안기전이매（ALT）、천문동안산안기전이매（AST）함량；간균장중병이철（MDA）、환원형곡광감태（GSH）적함량급간조직병이학변화；역전록PCR（RT-PCR）검측소서간장중종류배사인자α（TNF-α）、혈홍소가양매-1（HO-1）mRNA수평。결과：AP고제량조（100 mg/kg）강저소서혈청중ALT、AST수평，제고간조직중GSH활성，강저MDA수평，차이균유통계학의의（P＜0．05）；병리경검현시AP고제량조명현감경간손상；RT-PCR결과현시，AP고제량조TNF-α표체수평강저，이HO-1표체증강，차이균유통계학의의（P＜0．05）。결론：AP통과억제지질과양화반응，강저조직중양자유기적생성보호급성사록화탄간손상，기궤제가능여억제TNF-α적표체，유도HO-1표체유관。
Objective To investigate the role of andrographolide (AP) in protection of carbon tetrachloride (CCl4)-induced acute liver injury in mice and the possible mechanisms. Methods The mice were randomly divided into five groups, including two groups with different doses of AP (50 mg/kg and100 mg/kg), a control group, a CCl4 model group, and a silymarin group. Serum levels of alanine aminotransferase (ALT), aspartateminotransferase (AST), hepatic malondialdehyde (MDA), and glutathione (GSH) were examined. Pathological changes in the liver were observed. RT-PCR was used to detect the expressions of tumor necrosis factor-a (TNF-α) and heme oxygenase-1 (HO-1) mRNA. Results As compared with CCl4 model group, serum levels of ALT and AST and hepatic MDA activity were significantly decreased in AP group (100 mg·kg-1), along with a remarkable increase in hepatic GSH content. Pretreatment with AP at a high dose alleviated histopathological changes induced by CCl4. A markedly increased level of TNF-a induced by CCl4 was reduced by AP, while HO-1at transcriptional level was dramatically elevated following AP pretreatment. Conclusions AP plays a role in protection of CCl4-induced acute liver injury by inhibiting lipid peroxidation and reducing formation of free radicals, the mechanism may be involved in inhibition of TNF-αand activation of HO-1.