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Abstract：
Lambda-cyhalothrin (LCT) is a common pyrethroid insecticide widely used for ectoparasite control and hygiene pest prevention in poultry and this study aimed to investigate the mechanisms of LCT-induced cardiac injury in chickens. Low, medium, and high-dose LCT exposure models in chickens were established and hematoxylin and eosin (H&E) staining, dihydroethidium (DHE) staining, TUNEL staining, immunofluorescence, biochemical analysis, and gene expression analysis were used to study the effects of LCT exposure on the chicken heart. The results showed that LCT exposure increased the serum levels of creatine kinase (CK) and lactate dehydrogenase (LDH), led to muscle fiber breakage and inflammatory cell infiltration and caused cardiac tissue damage. The DHE staining and biochemical analysis revealed that LCT exposure resulted in the excessive accumulation of ROS, decreased activities/levels of catalase (CAT), total superoxide dismutase (T-SOD), and glutathione (GSH), and increased levels of the oxidative damage marker malondialdehyde (MDA). The TUNEL staining indicated that LCT exposure increased apoptosis possibly through the elevated expression of pro-apoptotic genes in the mitochondrial pathway, the reduced expression of anti-apoptotic genes, the upregulation of pro-inflammatory factors and the downregulation of anti-inflammatory factors. Here, LCT exposure significantly inhibited the expression of genes in the Nrf2/HO-1 pathway and activated the expression of genes in the CYP450 enzyme system. Compared to the low-dose group, the high-dose LCT exposure group showed lower levels of apoptosis and inflammation, possibly related to the low oxidative stress levels mediated by the decreased expression of the CYP450 enzyme system. In conclusion, LCT exposure induces oxidative stress, apoptosis, and inflammation in chicken hearts, which may be associated with the inhibition of the Nrf2/HO-1 pathway and activation of the CYP450 enzyme system. This study provides a theoretical basis for the safer use of insecticides in poultry production.
摘要：
λ-氯氟氰菊酯（LCT）是一种常见的拟除虫菊酯杀虫剂，广泛用于家禽的体外寄生虫控制和卫生害虫预防，本研究旨在探讨LCT引起的鸡心脏损伤的机制。Low,中等,建立鸡高剂量LCT暴露模型，并进行苏木精和伊红（H&E）染色，二氢乙锭(DHE)染色,TUNEL染色,免疫荧光，生化分析,和基因表达分析用于研究LCT暴露对鸡心脏的影响。结果表明，LCT暴露可使血清肌酸激酶（CK）和乳酸脱氢酶（LDH）水平升高，导致肌纤维断裂和炎症细胞浸润，引起心脏组织损伤。DHE染色和生化分析表明，LCT暴露导致ROS的过度积累，过氧化氢酶(CAT)活性/水平降低，总超氧化物歧化酶（T-SOD），和谷胱甘肽（GSH），氧化损伤标志物丙二醛（MDA）水平升高。TUNEL染色显示LCT暴露可能通过线粒体途径促凋亡基因的表达升高而增加细胞凋亡,抗凋亡基因的表达减少，促炎因子的上调和抗炎因子的下调。这里,LCT暴露显著抑制Nrf2/HO-1通路中基因的表达,激活CYP450酶系统中基因的表达。与低剂量组相比，高剂量LCT暴露组细胞凋亡和炎症水平较低，可能与CYP450酶系统表达降低介导的低氧化应激水平有关。总之,LCT暴露诱导氧化应激，凋亡，和鸡心脏的炎症，这可能与Nrf2/HO-1途径的抑制和CYP450酶系统的激活有关。本研究为在家禽生产中更安全地使用杀虫剂提供了理论依据。
