EGCG alleviated Mn exposure-caused carp kidney damage via trpm2-NLRP3-TNF-α-JNK pathway: Oxidative stress, inflammation, and tight junction dysfunction. Issue 134 (March 2023)

• Record Type: Journal Article
• Authors: Zhou, Qin; Cui, Jiawen; Liu, Yuhang; Gu, Lepeng; Teng, Xiaohua; Tang, You
• Is Part Of: Fish & shellfish immunology. Issue 134(2023)
• Publication Date: 2023-03
• Subjects: Manganese -- (−)-Epigallocatechin gallate -- Oxidative stress -- Inflammation -- Tight junction dysfunction; Fishes -- Immunology -- Periodicals; Shellfish -- Immunology -- Periodicals; Poissons -- Immunologie -- Périodiques; Crustacés -- Immunologie -- Périodiques; 571.9617
• DOI: 10.1016/j.fsi.2023.108582
• Languages: English
• ISSNs: 1050-4648

Abstract

Abstract: Manganese (Mn), an essential trace metal element in organisms. However, with extensive use of Mn in industry and agriculture, Mn becomes a heavy metal pollutant in water. (−)-epigallocatechin gallate (EGCG), an tea polyphenols, can alleviate metal toxicity. Kidney is an important detoxifying organ, but toxic mechanism of Mn to kidneys is unclear, which needs further research. Carp is an Asian important economical species for fisheries and a biological model for studying environmental toxicology. Thus, we established excess Mn and EGCG-supplemented carp model to explore molecular mechanism of EGCG alleviating Mn-caused carp kidney damage. In this experiment, we set a control group (the Con group), a Mn treatment group (the Mn group, 90 mg/L Mn), a EGCG supplement group (the EG group, 75 mg/kg EGCG), and a combined group (the Mn + EG group, 90 mg/L Mn and 75 mg/kg EGCG). Transcriptome, qRT-PCR, kit, and morphology method results indicated that excess Mn caused oxidative stress, inflammatory damage, and tight junction dysfunction in carp kidneys. Excess Mn-triggered oxidative stress caused tight junction dysfunction via trpm2-NLRP3-TNF-α-JNK pathway and inflammation. EGCG reversed the harm of Mn to fish through the above mechanism. The findings of this study provided the evidence of EGCG-alleviated Mn poisoning and offered new ideas for reducing heavy metal environmental pollution risk. Graphical abstract: Image 1 Highlights: For the first time we found that trpm6 took part in Mn exposure-caused OS. NLRP3 axis was involved in Mn treatment-caused inflammation. This is the first report that cpne2 participated in excess Mn-caused TJ dysfunction. Mn-caused OS, inflammation, and TJ dysfunction via trpm2-NLRP3-TNF-α-JNK. EGCG alleviated Mn-caused OS, inflammation, and TJ dysfunction in carp kidneys.