Department of Immunology, Medical Faculty of Niš, University of Nis, 18000 Niš, Serbia.
Clinic for Cardiovascular and Transplant Surgery, University Clinical Centre of Nis, 18000 Niš, Serbia.
Int J Mol Sci. 2024 Oct 15;25(20):11088. doi: 10.3390/ijms252011088.
Lipopolysaccharide (LPS) is known to induce oxidative stress and inflammation, leading to significant damage in cardiac tissues. This study investigates the protective effects of melatonin (MLT) against LPS-induced oxidative damage, inflammation, and apoptosis in rat heart tissue. Rats were divided into four groups ( = 6 per group): control, melatonin-treated, LPS-treated, and LPS + melatonin-treated. Oxidative stress markers, including thiobarbituric acid-reactive substances (TBARSs) and advanced oxidation protein products (AOPPs), were measured. Additionally, inflammatory markers, such as interleukin-6 (IL-6) levels, inducible nitric oxide synthase (iNOS) and nitric oxide (NO) content, and apoptotic markers, caspase-3, caspase-9, and acidic DNase activity, were evaluated. LPS treatment significantly increased TBARS, AOPP, and IL-6 levels, as well as the activity of caspase-3, acidic DNase and iNOS and NO content compared to the control group. Co-treatment with melatonin significantly reduced the levels of TBARS and AOPP levels, and caspase-3 and acidic DNase activities nearly matched those of the control group, while caspse-9 was still slightly increased. Interestingly, IL-6, iNOS and NO levels were significantly decreased but did not fully match the values in the control group. Melatonin mitigates LPS-induced oxidative stress, inflammation, and apoptosis in rat heart tissue by affecting all studied parameters, demonstrating its potential as a therapeutic agent for conditions characterized by oxidative stress and inflammation. Further research is warranted to explore the clinical applications of melatonin in cardiovascular diseases.
脂多糖（LPS）已知可诱导氧化应激和炎症，导致心脏组织的严重损伤。本研究探讨了褪黑素（MLT）对 LPS 诱导的大鼠心脏组织氧化损伤、炎症和细胞凋亡的保护作用。将大鼠分为四组（每组 n = 6）：对照组、褪黑素处理组、LPS 处理组和 LPS + 褪黑素处理组。测定了氧化应激标志物，包括硫代巴比妥酸反应物质（TBARSs）和晚期氧化蛋白产物（AOPPs）。此外，还评估了炎症标志物，如白细胞介素-6（IL-6）水平、诱导型一氧化氮合酶（iNOS）和一氧化氮（NO）含量，以及凋亡标志物 caspase-3、caspase-9 和酸性 DNase 活性。与对照组相比，LPS 处理组的 TBARS、AOPP 和 IL-6 水平以及 caspase-3、酸性 DNase 和 iNOS 的活性和 NO 含量显著升高。褪黑素联合治疗可显著降低 TBARS 和 AOPP 水平，caspase-3 和酸性 DNase 活性几乎与对照组相当，而 caspase-9 仍略有升高。有趣的是，IL-6、iNOS 和 NO 水平显著降低，但并未完全与对照组相匹配。褪黑素通过影响所有研究参数减轻 LPS 诱导的大鼠心脏组织氧化应激、炎症和细胞凋亡，表明其作为氧化应激和炎症特征疾病的治疗剂具有潜在应用价值。需要进一步研究探索褪黑素在心血管疾病中的临床应用。
