کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2595581 | 1562344 | 2013 | 8 صفحه PDF | دانلود رایگان |

• Wild type mice and TLR4-deficient mice are used for inducing myocardial damage model.
• We investigate whether TLR4 would be linked to myocardial damage due to PQ.
• TLR4-deficient mice are significantly resistant to the changes induced by PQ.
• The TLR4 plays an important role in myocardial damage due to PQ.
The ingestion of the herbicide paraquat (PQ) can cause multiple organ injury including cardiac lesions. However, the underlying mechanism of myocardial damage is not known. Toll-like receptor 4 (TRL4) is a pattern-recognition receptor in the innate immune response to microbial pathogens. TLR4 is involved in heart dysfunction such as septic shock or myocardial ischemia. We investigated whether TLR4 would be linked to the pathogenesis of heart disease due to PQ exposure. Wild type mice (WT) and TLR4-deficient mice were injected intraperitoneally with 75 mg/kg of PQ to induce myocardial damage and tested for echocardiographic assessment, histopathology, pro-inflammatory cytokine and TLR4 expression. WT mice after PQ exposure displayed deteriorate cardiac function, pathological damages, increased TLR4 mRNA and protein levels as well as myocardial TNF-α and IL-1β levels. Compared with WT mice, TLR4-deficient mice were significantly resistant to the PQ-induced injury. We concluded that the TLR4 was required as a mediator and played an important role in myocardial damage due to PQ.
Journal: Toxicology - Volume 312, 4 October 2013, Pages 115–122