Protective effect of pilose antler peptide on carbon tetrachloride-induced hepatotoxicity in mice

被引:38
作者
Ma Chunhua [1 ]
Long Hongyan [1 ]
机构
[1] Nanjing Univ TCM, Affiliated Hosp 3, Nanjing Municipal Hosp, Cent Lab, Nanjing 210001, Jiangsu, Peoples R China
关键词
Pilose antler peptide; Carbon tetrachloride hepatotoxicity; Inflammation; GROWTH-FACTOR-BETA; HEPATIC STELLATE CELLS; FACTOR-KAPPA-B; LIVER FIBROSIS; TGF-BETA; RATS; SIGNAL;
D O I
10.1016/j.ijbiomac.2017.03.024
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
The present study was designed to investigate the beneficial effects of pilose antler peptide (PAP) against carbon tetrachloride (CCl4) hepatotoxicity in mice, and explore the underlying mechanisms. In our results, animals were treated with either CCl4 and/or PAP for six consecutive weeks. The levels of inflammatory cytokines in serum and liver, hepatotoxicity markers in serum and histopathological evaluation were determined. PAP (50, 100 mg/kg) significantly inhibited the CCl4-incuded overproduction of inflammatory cytokines including tumor necrosis factor alpha (TNF-alpha), cytokines interleukin-1 beta (IL-1 beta), and interleukin-6 (IL-6) in serum and liver. Animals treated with PAP exhibited lower levels of alanine transaminase (ALT) and aspartate transaminase (AST), PAP administration alleviated CCl4 induced hepatic fibrosis as manifested in histopathological records. In fact, PAP prevented the activation of TLR/NF-kappa B pathway, by inhibiting the expression of TLR2, TLR4 MyD88, p-NF-kappa Bp65 and p-I kappa B alpha. In addition, PAP also significantly reversed CCl4-induced alteration of TGF-beta and p-samd-3 in liver tissue. In conclusion, PAP restored CCl4-induced hepatotoxicity via TLR/NF-kappa B and TGF-beta/samd-3 pathways. (C) 2017 Elsevier B.V. All rights reserved.
引用
收藏
页码:648 / 654
页数:7
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