Effect of chitosan on blood profile, inflammatory cytokines by activating TLR4/NF-κB signaling pathway in intestine of heat stressed mice.
Sahar Ghulam MohyuddinAftab QamarCan-Ying HuSheng-Wei ChenJia-Ying WenXiao-Xi LiuXing-Bin MaZhi-Chao YuYan-Hong YongLian-Yun WuMing-Long BaoXiang Hong JuPublished in: Scientific reports (2021)
Heat stress can significantly affect the immune function of the animal body. Heat stress stimulates oxidative stress in intestinal tissue and suppresses the immune responses of mice. The protecting effects of chitosan on heat stress induced colitis have not been reported. Therefore, the aim of this study was to investigate the protective effects of chitosan on immune function in heat stressed mice. Mice were exposed to heat stress (40 °C per day for 4 h) for 14 consecutive days. The mice (C57BL/6J), were randomly divided into three groups including: control group, heat stress, Chitosan group (LD: group 300 mg/kg/day, MD: 600 mg/kg/day, HD: 1000 mg/kg/day). The results showed that tissue histology was improved in chitosan groups than heat stress group. The current study showed that the mice with oral administration of chitosan groups had improved body performance as compared with the heat stress group. The results also showed that in chitosan treated groups the production of HSP70, TLR4, p65, TNF-α, and IL-10 was suppressed on day 1, 7, and 14 as compared to the heat stress group. In addition Claudin-2, and Occludin mRNA levels were upregulated in mice receiving chitosan on day 1, 7, and 14 of heat stress. Furthermore, the IL-6, IL-10, and TNF-α plasma levels were down-regulated on day 1, 7, and 14 of heat stress in mice receiving the oral administration of chitosan. In conclusion, the results showed that chitosan has an anti-inflammatory ability to tolerate hot environmental conditions.
Keyphrases
- heat stress
- drug delivery
- heat shock
- signaling pathway
- high fat diet induced
- oxidative stress
- wound healing
- immune response
- hyaluronic acid
- rheumatoid arthritis
- toll like receptor
- anti inflammatory
- inflammatory response
- type diabetes
- insulin resistance
- pi k akt
- epithelial mesenchymal transition
- skeletal muscle
- adipose tissue
- nuclear factor
- risk assessment
- cell proliferation
- lps induced
- ischemia reperfusion injury
- newly diagnosed
- endoplasmic reticulum stress
- heat shock protein