Abstract：
Lead acetate (PbAc) is a compound that produces toxicity in many tissues after exposure. Sinapic acid (SNP) possesses many biological and pharmacological properties. This study aimed to investigate the efficacy of SNP on the toxicity of PbAc in lung tissue. PbAc was administered orally at 30 mg/kg and SNP at 5 or 10 mg/kg for 7 days. Biochemical, genetic, and histological methods were used to investigate inflammatory, apoptotic, endoplasmic reticulum stress, and oxidative stress damage levels in lung tissue. SNP administration induced PbAc-reduced antioxidant (GSH, SOD, CAT, and GPx) and expression of HO-1 in lung tissue. It also reduced MDA, induced by PbAc, and thus alleviated oxidative stress. SNP decreased the inflammatory markers NF-κB, TNF-α and IL-1β levels induced by PbAc in lung tissue and exhibited anti-inflammatory effect. PbAc increased apoptotic Bax, Apaf-1, and Caspase-3 mRNA transcription levels and decreased anti-apoptotic Bcl-2 in lung tissues. SNP decreased apoptotic damage by reversing this situation. On the other hand, SNP regulated these markers and brought them closer to the levels of the control group. PbAc caused prolonged ER stress by increasing the levels of ATF6, PERK, IRE1α, GRP78 and this activity was stopped and tended to retreat with SNP. After evaluating all the data, While PbAc caused toxic damage in lung tissue, SNP showed a protective effect by reducing this damage.
摘要：
醋酸铅（PbAc）是一种在暴露后在许多组织中产生毒性的化合物。芥子酸（SNP）具有许多生物学和药理学特性。本研究旨在探讨SNP对PbAc肺组织毒性的影响。PbAc以30mg/kg口服给药,SNP以5或10mg/kg口服给药7天。生物化学,遗传,和组织学方法用于研究炎症，凋亡，内质网应激,肺组织氧化应激损伤水平。SNP给药诱导PbAc降低的抗氧化剂（GSH，SOD,CAT,和GPx）和HO-1在肺组织中的表达。它还减少了MDA，由PbAc诱导，从而减轻了氧化应激。SNP降低炎症标志物NF-κB，PbAc诱导肺组织中TNF-α和IL-1β水平变化并表现出抗炎作用。PbAc增加凋亡Bax，肺组织中Apaf-1和Caspase-3mRNA转录水平和抗凋亡Bcl-2降低。SNP通过逆转这种情况减少了凋亡损伤。另一方面,SNP调节这些标记并使它们更接近对照组的水平。PbAc通过增加ATF6、PERK、IRE1α,GRP78和该活动被停止并且倾向于随着SNP而撤退。在评估了所有数据之后，虽然PbAc在肺组织中引起毒性损伤，SNP通过减少这种损伤而显示出保护作用。
