Chronic oral exposure to cadmium causes liver inflammation by NLRP3 inflammasome activation in pubertal mice
| Autor: | Haiwei Li, Jietian Jin, Jianxia Sun, Xinwei Jiang, Zhenhua Li, Lingmin Tian, Guobing Chen, Weibin Bai, Xusheng Li, Ping Li, Dongbao Cai |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
medicine.medical_specialty
Inflammasomes Administration Oral Inflammation Apoptosis Cadmium chloride Toxicology medicine.disease_cause Hepatitis 03 medical and health sciences chemistry.chemical_compound Mice 0404 agricultural biotechnology Cadmium Chloride Internal medicine NLR Family Pyrin Domain-Containing 3 Protein medicine Macrophage Animals Transaminases 030304 developmental biology Liver injury 0303 health sciences business.industry Macrophages Puberty Inflammasome 04 agricultural and veterinary sciences General Medicine Macrophage Activation medicine.disease 040401 food science Up-Regulation Endocrinology medicine.anatomical_structure chemistry Liver Hepatocyte Cytokines Liver function medicine.symptom business Oxidative stress Food Science medicine.drug |
| Zdroj: | Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association. 148 |
| ISSN: | 1873-6351 |
| Popis: | Cadmium (Cd) is a potentially toxic trace element frequently existed in foods, water, and air, threatening liver function from its continuous bioaccumulation and induction of oxidative stress and inflammation. However, the hepatotoxicity of Cd during puberty remains unclear. In this study, pubertal mice were given cadmium chloride at a dose of 5.0 mg/kg·bw by gavage, and the liver damage was investigated at different treatment points of 10, 20, and 30 days. After Cd exposure, there is an obvious inflammatory hepatocyte infiltration accompanied by more apoptotic cells at 20 days and an increase in alanine aminotransferases and aspartate aminotransferases in circulation at 30 days. Additionally, the soaring TNF-α and MCP-1 were found in liver, and the mRNA expression of pro-inflammatory cytokines (IL-1α, IL-1β, and IL-18) and anti-inflammatory cytokines (TGF-β, IL-10, and IL-13) were both significantly upregulated. Moreover, the activated M1 and M2 macrophages were confirmed in charge of these cytokines release. Most importantly, the data validated a pivotal role of NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome in Cd-induced inflammation in liver at puberty. Collectively, our results suggested that low-dose Cd oral exposure can cause liver inflammation via activation of NLRP3 inflammasome and give rise to severe liver injury at puberty. |
| Databáze: | OpenAIRE |
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