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Abstract Title:

Oridonin ameliorates lipopolysaccharide/D-galactosamine-induced acute liver injury in mice via inhibition of apoptosis.

Abstract Source:

Am J Transl Res. 2017 ;9(9):4271-4279. Epub 2017 Sep 15. PMID: 28979700

Abstract Author(s):

Yilin Deng, Chen Chen, Heguo Yu, Hua Diao, Cuicui Shi, Yugang Wang, Guangming Li, Min Shi

Article Affiliation:

Yilin Deng

Abstract:

We investigated the protective effects exerted by oridonin, the main active constituent of the Chinese medicinal herb, against lipopolysaccharide (LPS)/D-galactosamine (D-Gal)-induced acute liver injury (ALI). An ALI model was induced in mice using LPS (40μg/0.5 ml) and D-Gal (5 mg/0.5 ml). The mice were randomly divided into the following five groups of six mice each: one control group (a), one ALI group (b), two oridonin treatment groups (c and d), and one oridonin control group (e). Oridonin (0.2 mg/0.5 ml) was administered once 1 h prior to theLPS/D-Gal challenge in group c and a total of three times over a period of four days, with the last dose given at 1 h before the LPS/D-Gal challenge, in group d. Pretreatment with oridonin improved the survival rate, alleviated histopathological abnormalities, and suppressed plasma aminotransferasesin the LPS/D-Gal-challenged mice. Importantly, oridonin attenuated LPS/D-Gal-induced apoptosis in hepatocytes by reducing pro-apoptotic signals (P<0.05), such as tumor necrosis factor-α (TNF-α) and c-Jun N-terminal kinases (JNK). Furthermore, JNK-associated mitochondrial pro-apoptotic proteins were also suppressed by pretreatment with oridonin. Taken together, these data show that oridonin exerts protective effects against LPS/D-Gal-induced ALI in mice via a mechanism that mayinvolve the suppression of the pro-apoptotic cytokine TNF-α and JNK-associated pro-apoptotic signaling.

Study Type : Animal Study

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