Grape seed proanthocyanidin extract alleviates inflammation in experimental colitis mice by inhibiting NF-κB signaling pathway

被引:8
作者
Chu, Lei [1 ,2 ]
Zhang, Shaoru [1 ,2 ,3 ,4 ]
Wu, Weidong [1 ,2 ]
Gong, Yuqing [3 ,4 ]
Chen, Zhenshi [1 ,2 ]
Wen, Yanting [3 ,4 ]
Wang, Yong [3 ,4 ,5 ,6 ]
Wang, Lihui [3 ,4 ,5 ,6 ]
机构
[1] Nantong Univ, Peoples Hosp Danyang, Clin Lab, Danyang, Peoples R China
[2] Nantong Univ, Affiliated Danyang Hosp, Danyang, Peoples R China
[3] Nanjing Univ, Med Sch, State Key Lab Analyt Chem Life Sci, Nanjing, Peoples R China
[4] Nanjing Univ, Med Sch, Jiangsu Key Lab Mol Med, Nanjing, Peoples R China
[5] Nanjing Univ, Med Sch, State Key Lab Analyt Chem Life Sci & Jiangsu Key L, Nanjing 210093, Peoples R China
[6] Nanjing Univ, Med Sch, Jiangsu Key Lab Mol Med, Nanjing 210093, Peoples R China
基金
中国国家自然科学基金;
关键词
grape seed proanthocyanidin extract; inflammation; NF-kappa B signaling pathway; RAW264.7; ulcerative colitis; SULFATE-INDUCED COLITIS; ULCERATIVE-COLITIS; PROCYANIDIN EXTRACT; COLORECTAL-CANCER; DAMAGE;
D O I
10.1002/tox.24129
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
Ulcerative colitis (UC) is a complex inflammatory disease of colorectum that induces abnormal immune responses and severely affects the quality of life of the patients. Grape seed proanthocyanidin extract (GSPE) exerts anti-inflammatory and antioxidant functions in many inflammatory diseases. The objective of this study was to investigate the potential therapeutic effects and underlying mechanisms of GSPE in UC using a dextran sodium sulfate (DSS)-induced mouse UC model and a lipopolysaccharide (LPS)-stimulated RAW264.7 macrophage model. In this study, we found that the GSPE markedly prevented DSS-induced weight loss and colon length shortening in UC mice. Further investigations showed that GSPE significantly attenuated the expression of pro-inflammatory cytokines TNF-alpha, IL-6, and IL-1 beta, and elevated the expression of anti-inflammatory cytokine IL-10 in the colon tissues and serum of DSS-induced colitis mice by suppressing NF-kappa B signaling pathway. Furthermore, LPS-induced inflammation in RAW264.7 cells was also reversed by GSPE. Taken together, our results confirm that GSPE can ameliorate inflammatory response in experimental colitis via inhibiting NF-kappa B signaling pathway. This study advances the research progress on a potentially effective therapeutic strategy for inflammatory bowel diseases.
引用
收藏
页码:2572 / 2582
页数:11
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