Background

Oxidative stress is involved in the pathogenesis of various inflammatory diseases, such as periodontitis. When periodontitis occurs, reactive oxygen species (ROS) are overproduced and cannot be balanced by the antioxidant defense system, resulting in tissue damage. Madecassic acid (MA), an abundant triterpenoid in Centella asiatica (L.) Urban, has been used as a wound healing, antiinflammatory, and anticancer agent. Moreover, recent studies have shown that MA has an antioxidative effect, but the underlying mechanism remains unclear.

Objective

Here, we established an effective oxidative stress model induced by hydrogen peroxide (H₂O₂) in human periodontal ligament fibroblasts (hPDLFs) to investigate the antioxidant and protective effects of MA against cell damage and its underlying mechanism of action.

Results

Pretreatment with MA inhibited cell apoptosis and promoted cell invasion and migration against oxidative injury induced by H₂O₂. In addition, MA was able to maintain mitochondrial membrane potential (ΔΨm) under oxidative stress. Notably, we found that MA restored redox balance by reducing intracellular ROS production. Furthermore, we investigated apoptosis-related proteins and found that the levels of anti-apoptosis markers Bcl-xL and Bcl-2 were remarkably upregulated, whereas that of the pro-apoptotic marker Bax was strikingly downregulated.

Conclusions

Collectively, these findings suggest that MA inhibits H₂O₂-induced oxidative stress and apoptosis of hPDLFs by reducing intracellular ROS production to maintain ΔΨm stability.

中文翻译：

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Madecassic acid 通过维持线粒体膜电位保护人牙周膜成纤维细胞免受过氧化氢诱导的细胞损伤

背景

氧化应激参与了牙周炎等多种炎症性疾病的发病机制。当牙周炎发生时，活性氧（ROS）过量产生，无法被抗氧化防御系统平衡，导致组织损伤。Madecassic acid (MA) 是积雪草(L.) Urban 中丰富的三萜类化合物，已被用作伤口愈合、抗炎和抗癌剂。此外，最近的研究表明 MA 具有抗氧化作用，但其潜在机制尚不清楚。

客观的

在这里，我们在人牙周膜成纤维细胞 (hPDLFs) 中建立了过氧化氢 (H ₂ O ₂ )诱导的有效氧化应激模型，以研究 MA 对细胞损伤的抗氧化和保护作用及其潜在作用机制。

结果

MA预处理抑制细胞凋亡，促进细胞侵袭和迁移，对抗H ₂ O ₂诱导的氧化损伤。此外，MA 能够在氧化应激下维持线粒体膜电位 (ΔΨm)。值得注意的是，我们发现 MA 通过减少细胞内 ROS 的产生来恢复氧化还原平衡。此外，我们研究了凋亡相关蛋白，发现抗凋亡标志物 Bcl-xL 和 Bcl-2 的水平显着上调，而促凋亡标志物 Bax 的水平显着下调。

结论

总的来说，这些发现表明 MA通过减少细胞内 ROS 的产生来维持 ΔΨm 的稳定性，从而抑制 H ₂ O ₂诱导的 hPDLF 的氧化应激和细胞凋亡。