아세트아미노펜으로 유도된 간독성에 대한 계혈등 물추출물의 간세포 보호효과 (Hepatoprotective Activity of Spatholobi Caulis Water Extract against Acetaminophen-induced Toxicity in Rats)

서지정보

· 발행기관 : 대한본초학회
· 수록지 정보 : 대한본초학회지 / 26권 / 3호 / 65 ~ 73페이지
· 저자명 : 이인우, 최홍식, 김승모

초록

Objectives：The present study was evaluated the protective roles of Spatholobi Caulis in hepatotoxic rats due to APAP overdose.
Methods：In experiments, rats were orally administrated with the aqueous extract of Spatholobi Caulis (SCE;50, 100 mg/kg) for 4 days and then, orally gavage with APAP (1.2 g/kg) to induce acute liver damage.
Results：Oral injection of APAP caused severe hepatic injury. Plasma ALT, AST and LDH levels were significantly elevated, but SCE significantly decreased ALT, AST and LDH to the normal level. In histopathological analysis, peripheral hemorrhage around portal triads and central necrosis around central veins were founded after APAP treatment. However, these histopathological changes were recovered by SCE pretreatment. SCE also decreased the percentage of generative hepatic regions (%/㎟ hepatic parenchyma), the numbers of inflammatory cells (cells/㎟ hepatic parenchyma) and the number of degenerative hepatic cells (N/100 hepatic cellls) which were significantly elevated after APAP injection. Furthermore, SCE down-regulated the contents of hepatic MDA and up-regulated hepatic GSH. SCE also inhibited the decrease in the expression of pro-caspase-3 by APAP treatment.
Conclusions：Collectively, these data indicate that SCE protected APAP-induced hapatic damages through antioxidative and anti-apoptotic process. These findings the significant therapeutic potential of SCE during APAP-induced liver injury.

영어초록

Objectives：The present study was evaluated the protective roles of Spatholobi Caulis in hepatotoxic rats due to APAP overdose.
Methods：In experiments, rats were orally administrated with the aqueous extract of Spatholobi Caulis (SCE;50, 100 mg/kg) for 4 days and then, orally gavage with APAP (1.2 g/kg) to induce acute liver damage.
Results：Oral injection of APAP caused severe hepatic injury. Plasma ALT, AST and LDH levels were significantly elevated, but SCE significantly decreased ALT, AST and LDH to the normal level. In histopathological analysis, peripheral hemorrhage around portal triads and central necrosis around central veins were founded after APAP treatment. However, these histopathological changes were recovered by SCE pretreatment. SCE also decreased the percentage of generative hepatic regions (%/㎟ hepatic parenchyma), the numbers of inflammatory cells (cells/㎟ hepatic parenchyma) and the number of degenerative hepatic cells (N/100 hepatic cellls) which were significantly elevated after APAP injection. Furthermore, SCE down-regulated the contents of hepatic MDA and up-regulated hepatic GSH. SCE also inhibited the decrease in the expression of pro-caspase-3 by APAP treatment.
Conclusions：Collectively, these data indicate that SCE protected APAP-induced hapatic damages through antioxidative and anti-apoptotic process. These findings the significant therapeutic potential of SCE during APAP-induced liver injury.

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