Mercuric chloride (HgCl2) is extremely toxic to both humans and animals. It could be absorbed via ingestion, inhalation, and skin contact. Exposure to HgCl2 can cause severe health effects, including damages to the gastrointestinal, respiratory, and central nervous systems. The purpose of this work was to explore if carvacrol (CRV) could protect rats lungs from damage caused by HgCl2. Intraperitoneal injections of HgCl2 at a dose of 1.23 mg/kg body weight were given either alone or in conjunction with oral CRV administration at doses of 25 and 50 mg/kg body weight for 7 days. The study included biochemical and histological techniques to examine the lung tissue's oxidative stress, apoptosis, inflammation, and autophagy processes. HgCl2‐induced reductions in GSH levels and antioxidant enzymes (SOD, CAT, and GPx) activity were enhanced by CRV co‐administration. Furthermore, MDA levels were lowered by CRV. The inflammatory mediators NF‐κB, IκB, NLRP3, TNF‐α, IL‐1β, IL6, COX‐2, and iNOS were all reduced by CRV. When exposed to HgCl2, the levels of apoptotic Bax, caspase‐3, Apaf1, p53, caspase‐6, and caspase‐9 increased, but the levels of antiapoptotic Bcl‐2 reduced after CRV treatment. CRV decreased levels of Beclin‐1, LC3A, and LC3B, which in turn decreased HgCl2‐induced autophagy damage. After HgCl2 treatment, higher pathological damage was observed in terms of alveolar septal thickening, congestion, edema, and inflammatory cell infiltration compared to the control group while CRV ameliorated these effects. Consequently, by preventing HgCl2‐induced increases in oxidative stress and the corresponding inflammation, autophagy, apoptosis, and disturbance of tissue integrity in lung tissues, CRV might be seen as a useful therapeutic alternative.

中文翻译：

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香芹酚通过调节氧化应激、细胞凋亡、炎症和自噬对氯化汞诱导的肺毒性的保护作用


氯化汞 （HgCl2） 对人类和动物都有极强的毒性。它可以通过摄入、吸入和皮肤接触吸收。接触 HgCl2 会对健康造成严重影响，包括对胃肠道、呼吸系统和中枢神经系统的损害。这项工作的目的是探讨香芹酚 （CRV） 是否可以保护大鼠肺部免受 HgCl2 造成的损害。以 1.23 mg/kg 体重的剂量腹腔注射 HgCl2 单独给药或以 25 和 50 mg/kg 体重的剂量与口服 CRV 联合给药，持续 7 天。该研究包括生化和组织学技术，以检查肺组织的氧化应激、细胞凋亡、炎症和自噬过程。CRV 联合给药增强了 HgCl2 诱导的 GSH 水平和抗氧化酶 （SOD、CAT 和 GPx） 活性的降低。此外，CRV 降低了 MDA 水平。炎症介质 NF-κB 、 IκB 、 NLRP3 、 TNF-α 、 IL-1β 、 IL6 、 COX-2 和 iNOS 均被 CRV 降低。当暴露于 HgCl2 时，凋亡 Bax 、 caspase-3 、 Apaf1 、 p53 、 caspase-6 和 caspase-9 的水平增加，但 CRV 处理后抗凋亡 Bcl-2 的水平降低。CRV 降低了 Beclin-1 、 LC3A 和 LC3B 的水平，进而减少了 HgCl2 诱导的自噬损伤。HgCl2 治疗后，与对照组相比，在肺泡间隔增厚、充血、水肿和炎性细胞浸润方面观察到更高的病理损伤，而 CRV 改善了这些影响。因此，通过防止 HgCl2 诱导的氧化应激增加和相应的炎症、自噬、细胞凋亡和肺组织中组织完整性的紊乱，CRV 可能被视为一种有用的治疗选择。