Preinduced intestinal HSP70 improves visceral hypersensitivity and abnormal intestinal motility in PI-IBS mouse model

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• 作者：Cheng Lan¹ ; ^{lancheng71@163.com" class="auth_mail" title="E-mail the corresponding author} ; Xiao-Ning Sun¹ ; Xu-Chun Zhou¹ ; Bo Yang² ; Bai-Li Huang¹ ; Tao-Zhi Deng¹ ; Zhou-Tao He¹ ; Xiang-Yang Han¹
• 关键词：Post-infectious irritable bowel syndrome ; Heat shock protein 70 ; Proinflammatory cytokine ; Visceral hypersensitivity ; Intestinal motility
• 刊名：Asian Pacific Journal of Tropical Medicine
• 出版年：2016
• 出版时间：March 2016
• 年：2016
• 卷：9
• 期：3
• 页码：302-305
• 全文大小：363 K

文摘

To investigate the impact of the preinduced intestinal heat shock protein 70 (HSP70) on the visceral hypersensitivity and abnormal intestinal motility in a post-infectious irritable bowel syndrome (PI-IBS) mouse model.

Methods

Eighty-four female C57BL/6 mice were randomly assigned to four groups: control group (n = 21) and induction + PI-IBS group (n = 21), PI-IBS group (n = 21) and induction group (n = 21). The mice in PI-IBS group were infected in vivo with Trichinella spiralis by oral administration. The visceral hypersensitivity and intestinal motility were evaluated respectively with abdominal withdrawal reflex and colon transportation test. The intestinal HSP70 protein and mRNA level was measured by Western blot and real-time PCR. Meanwhile, the intestinal proinflammatory cytokines IL-10 and TNF-α level was detected by ELISA.

Results

Compared with their counterparts in PI-IBS group, the animals in the Induction + PI-IBS group show significantly increased intestinal level of HSP70 and obviously ameliorative clinical figures, including abdominal withdrawal reflex score, intestine transportation time and Bristol scores (P < 0.05). Meanwhile, the intestinal post-inflammatory cytokines remarkably changed, including increased IL-10 level and decreased TNF-α level (P < 0.05).

Conclusions

Intestinal HSP70 may play a potential protective role through improving the imbalance between the intestinal post-inflammatory and anti-inflammatory cytokines in PI-IBS.