2. Academic Validation
  3. Melatonin ameliorates imidacloprid-induced intestinal injury by negatively regulating the PGN/P38MAPK pathway in the common carp (Cyprinuscarpio)

Melatonin ameliorates imidacloprid-induced intestinal injury by negatively regulating the PGN/P38MAPK pathway in the common carp (Cyprinuscarpio)

  • Fish Shellfish Immunol. 2022 Dec:131:1063-1074. doi: 10.1016/j.fsi.2022.11.018.
Zhiruo Miao 1,  Zhiying Miao 2,  Min Liu 3,  Shiwen Xu 4
Affiliations

Affiliations

  • 1 College of Animal Science and Technology, Northeast Agricultural University, Harbin, 150030, PR China.
  • 2 College of Life Science, Northeast Agricultural University, Harbin, 150030, PR China.
  • 3 College of Animal Science and Technology, Northeast Agricultural University, Harbin, 150030, PR China. Electronic address: [email protected].
  • 4 College of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, PR China; Key Laboratory of the Provincial Education Department of Heilongjiang for Common Animal Disease Prevention and Treatment, College of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, PR China. Electronic address: [email protected].
PMID: 36375784 DOI: 10.1016/j.fsi.2022.11.018
Abstract

Imidacloprid (IMI), one of the most frequently used neonicotinoid insecticides in agriculture, is resided in surface water worldwide and poses a threat to aquatic organisms. Melatonin (MT) provides effective protection against insecticide-induced toxicity, nevertheless, the toxic effects and whether MT attenuates intestinal injury caused by IMI exposure in the common carps remains poorly explored. Previous studies have reported adverse effects of IMI exposure on intestinal health status. Therefore, we first demonstrated that IMI altered the composition and function of the intestinal microbiota, destroying the integrity of intestinal ultrastructure, increasing intestinal permeability. Meanwhile, metagenomic Sequencing and ELISA kits results hypothesized that peptidoglycan (PGN) is an IMI-triggered intestinal microbial metabolite. Subsequently, we thus further elucidated that IMI induced an increase in intestinal tight junction permeability by inducing PGN secretion in vitro model. MT addition dramatically attenuated IMI-induced intestinal toxicity by remitting PGN synthesis and thus resecuring tight junction permeability, thereby reducing intestinal injury. SB203580 was supplied as a P38MAPK inhibitor to alleviate the increased permeability of tight junctions induced by IMI/PGN. Therefore, these findings confirmed that MT protects against IMI-induced intestinal injury by negatively regulating PGN/P38MAPK pathway to antagonize the increased tight junction permeability.

Keywords

Imidacloprid; Intestinal microbiota; Melatonin; PGN / P38MAPK pathway; Tight junction permeability.

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