Chitosan-gentamicin conjugate attenuates heat stress-induced intestinal barrier injury via the TLR4/STAT6/MYLK signaling pathway: In vitro and in vivo studies

Niu, Xueting; Hu, Canying; Chen, Shengwei; Wen, Jiaying; Liu, Xiaoxi; Yong, Yanhong; Yu, Zhichao; Ma, Xingbin; Li, Chengpeng; Warda, MOHAMAD; HASSIBELNABY, ABDELATY; Gooneratne, Ravi; Ju, Xianghong

doi:10.1016/j.carbpol.2023.121279

Chitosan-gentamicin conjugate attenuates heat stress-induced intestinal barrier injury via the TLR4/STAT6/MYLK signaling pathway: In vitro and in vivo studies

Niu X., Hu C., Chen S., Wen J., Liu X., Yong Y., ...Daha Fazla

Carbohydrate Polymers, cilt.321, 2023 (SCI-Expanded, Scopus)

Yayın Türü: Makale / Tam Makale
Cilt numarası: 321
Basım Tarihi: 2023
Doi Numarası: 10.1016/j.carbpol.2023.121279
Dergi Adı: Carbohydrate Polymers
Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, PASCAL, BIOSIS, Biotechnology Research Abstracts, CAB Abstracts, Chemical Abstracts Core, Chimica, Compendex, EMBASE, Food Science & Technology Abstracts, Veterinary Science Database
Anahtar Kelimeler: CS-GT, Heat stress, Intestinal barrier injury, TLR4/STAT6/MYLK
Atatürk Üniversitesi Adresli: Evet

Özet

Heat stress (HS) has a negative impact on animal health. A modified chitosan-gentamicin conjugate (CS-GT) was prepared to investigate its potential protective effects and mechanism of action on heat stress-induced intestinal mucosa injury in IPEC-J2 cells and mouse 3D intestinal organs in a mouse model. CS-GT significantly (P < 0.01) reversed the decline in transmembrane resistance and increased the FITC-dextran permeability of the IPEC-J2 monolayer fusion epithelium caused by heat stress. Heat stress decreased the expression of the tight binding proteins occludin, claudin1, and claudin2. However, pretreatment with CS-GT significantly increased (P < 0.01) the expression of these tight binding proteins. Mechanistically, CS-GT inhibited the activation of the TLR4/STAT6/MYLK signaling pathway induced by heat stress. Molecular docking showed that CS-GT can bind effectively with TLR4. In conclusion, CS-GT alleviates heat stress-induced intestinal mucosal damage both in vitro and in vivo. This effect is mediated, at least partly, by the inhibition of the TLR4/STAT6/MYLK signaling pathway and upregulation of tight junction proteins. These findings suggest that CS-GT may have therapeutic potential in the prevention and treatment of heat stress-related intestinal injury.