It has been shown that near all organs, especially the cardiovascular system, are affected by bacterial lipopolysaccharide via the activation of Toll-like receptor signaling pathways. Here, we tried to find the blunting effect of bacterial lipase on lipopolysaccharide (LPS)-induced cardiac tissue toxicity in chicken embryos. 7-day fertilized chicken eggs were divided randomly into different groups as follows; Control, Normal Saline, LPS (0.1, 0.5 and 1 mg/kbw), and LPS (0.1, 0.5 and 1 mg/kbw) plus 5 mg/ml Lipase. On day 17, the hearts were sampled. The expression of genes such as GATA4, NKX2.5, EGFR, TRIF, and NF-ƙB was monitored using real-time PCR analysis. Using western blotting, we measured NF-ƙB protein level. Total antioxidant capacity, glutathione peroxidase, and Catalase activity were also studied. Microvascular density and anterior wall thickness were monitored in histological samples using H&E staining. High dose of LPS (1 mg/kbw) increased the expression of TRIF but not NF-ƙB compared to the control group (p < 0.05). We found a statistically significant reduction in groups that received LPS + Lipase compared to the control and LPS groups (p < 0.05). Western blotting revealed that the injection of Lipase could reduce LPS-induced NF-ƙB compared to the control group (p < 0.05). The expression of GATA4, NKx2.5, and EGFR was not altered in the LPS group, while the simultaneous application of LPS and Lipase significantly reduced GATA4, NKx2.5, and EGFR levels below the control (p < 0.05). We found non-significant differences in glutathione peroxidase, and Catalase activity in all groups (p > 0.05), while total antioxidant capacity was increased in groups that received LPS + Lipase. Anterior wall thickness was diminished in LPS groups and the use of both lipase and LPS returned near-to-control values (p < 0.05). Despite a slight increase in microvascular density, we found statistically non-significant differences in all groups (p > 0.05). Bacterial lipase reduces detrimental effects of LPS on chicken embryo heart induced via Toll-like receptor signaling pathway.

已经表明，在所有器官附近，尤其是心血管系统，都受到细菌脂多糖通过激活 Toll 样受体信号通路的影响。在这里，我们试图发现细菌脂肪酶对脂多糖 (LPS) 诱导的鸡胚心脏组织毒性的钝化作用。7天受精鸡蛋随机分为以下不同组；对照、生理盐水、LPS（0.1、0.5 和 1 mg/kbw）和 LPS（0.1、0.5 和 1 mg/kbw）加 5 mg/ml 脂肪酶。第 17 天，对心脏进行取样。使用实时 PCR 分析监测 GATA4、NKX2.5、EGFR、TRIF 和 NF-ƙB 等基因的表达。使用蛋白质印迹，我们测量了 NF-ƙB 蛋白水平。还研究了总抗氧化能力、谷胱甘肽过氧化物酶和过氧化氢酶活性。使用 H&E 染色监测组织学样品中的微血管密度和前壁厚度。与对照组相比，高剂量 LPS (1 mg/kbw) 增加了 TRIF 但不增加 NF-ƙB 的表达 (p < 0.05)。我们发现，与对照组和 LPS 组相比，接受 LPS + 脂肪酶的组有统计学意义的减少（p  < 0.05)。Western blotting显示，与对照组相比，注射Lipase可降低LPS诱导的NF-ƙB（p  < 0.05）。LPS组GATA4、NKx2.5和EGFR的表达没有改变，而同时应用LPS和脂肪酶显着降低了GATA4、NKx2.5和EGFR的水平，低于对照组（p  < 0.05）。我们发现所有组的谷胱甘肽过氧化物酶和过氧化氢酶活性没有显着差异（p  > 0.05），而接受LPS +脂肪酶的组的总抗氧化能力增加。LPS 组的前壁厚度减少，脂肪酶和 LPS 的使用返回接近控制值（p < 0.05)。尽管微血管密度略有增加，但我们发现所有组的差异无统计学意义（p  > 0.05）。细菌脂肪酶可降低 LPS 对通过 Toll 样受体信号通路诱导的鸡胚心脏的不利影响。