This study addresses the effect of D‐galactose‐induced toxicity associated senescence mitigated by alpinate oxyphyllae fructus (AOF; Alpinia oxyphylla Miq) extracts fortified with adipose‐derived mesenchymal stem cells (ADMSCs) in rats. Male 18 week‐old Wistar Kyoto (WKY) rats were used in this study. We analyzed cardiac fibrosis by Masson's trichrome staining. The tissue sections were dyed using hematoxylin and eosin (H&E). Tissue sections were stained for the restoration of Nrf2 expression in treatment groups by immunohistochemistry. Immunohistochemistry and western blotting analysis showed that AOF with ADMSCs could significantly reduce aging‐induced oxidative stress in D‐galactose‐induced aging rat hearts by inducing Nrf2 pathway. Reduction in ROS resulted in the suppression of inflammatory signals (p‐NF‐κB and IL‐6). Histopathological studies were showed an increased interstitium and collagen accumulation in aging‐induced heart sections. However, AOF and ADMSCs treated hearts were recovered from cardiac remodeling. Furthermore, hypertrophy and fibrosis associated markers were also significantly reduced (P < .05) in treatment groups. We speculate that ADMSCs might activate certain paracrine factors, which could target the upstream activator of aging associated cardiac complications and AOF might provide homing for these stem cells.

中文翻译：

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高山酸益茶强化脂肪间充质干细胞可减轻 D-半乳糖诱导的衰老相关毒性

本研究探讨了用脂肪源性间充质干细胞 (ADMSC) 强化的高山益智 (AOF; Alpinia oxyphylla Miq) 提取物减轻 D-半乳糖诱导的与衰老相关的毒性的作用。本研究使用 18 周龄雄性 Wistar京都 (WKY) 大鼠。我们通过马森三色染色分析了心脏纤维化。使用苏木精和曙红（H&E）对组织切片进行染色。通过免疫组织化学对组织切片进行染色以观察治疗组中 Nrf2 表达的恢复情况。免疫组织化学和蛋白质印迹分析表明，AOF 与 ADMSCs 可以通过诱导 Nrf2 通路，显着降低 D-半乳糖诱导的衰老大鼠心脏中衰老引起的氧化应激。ROS 的减少导致炎症信号（p-NF-κB 和 IL-6）的抑制。组织病理学研究表明，衰老引起的心脏切片中间质和胶原蛋白积累增加。然而，经 AOF 和 ADMSC 处理的心脏可从心脏重塑中恢复。此外，治疗组中肥厚和纤维化相关标志物也显着减少（P < .05）。我们推测 ADMSC 可能会激活某些旁分泌因子，这些因子可能会靶向衰老相关心脏并发症的上游激活因子，而 AOF 可能会为这些干细胞提供归巢。