Abstract Plantamajoside (PMS) is a phenylpropanoid glycoside that possesses anti-diabetic activity. However, the effect of PMS on diabetic nephropathy (DN) has not been investigated. This study aimed to evaluate the role of PMS in DN and the potential mechanism. The rat glomerular mesangial cells ((MCs) (HBZY-1 cells) were cultured under high glucose (HG) condition or normal condition with or without the treatment of PMS. The results showed that PMS ameliorated the cell injury that was induced by HG in HBZY-1 cells. The HG-caused increases in reactive oxygen species (ROS) and malondialdehyde (MDA) production and decrease in superoxide dismutase (SOD) activity were prevented by PMS. The qRT-PCR and ELISA assays demonstrated an anti-inflammatory activity of PMS, as evidenced by decreased levels of TNF-α, IL-1β, and IL-6 in HG-induced HBZY-1 cells. Moreover, the increased levels of fibronectin (FN) and collagen type IV (Col IV) in HBZY-1 cells caused by HG were also reduced by PMS treatment. Furthermore, PMS significantly suppressed HG-induced activation of Akt/NF-κB signaling in HBZY-1 cells. Taken together, these findings indicated that PMS alleviated HG-induced injury in HBZY-1 cells through suppressing oxidative stress, inflammatory response, and extracellular matrix (ECM) accumulation via the inactivating Akt/NF-κB pathway. Thus, PMS might possess potential capacity for the treatment of DN.

中文翻译：

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Plantamajoside 通过 Akt/NF-κB 通路的失活抑制大鼠肾小球系膜细胞中高糖诱导的氧化应激、炎症和细胞外基质积累

摘要 Plantamajoside (PMS) 是一种苯丙醇苷，具有抗糖尿病活性。然而，PMS 对糖尿病肾病 (DN) 的影响尚未得到研究。本研究旨在评估 PMS 在 DN 中的作用及其潜在机制。大鼠肾小球系膜细胞（（MCs）（HBZY-1 细胞）在高糖（HG）条件或正常条件下，有或无 PMS 处理，结果显示 PMS 改善了 HG 诱导的细胞损伤。 HBZY-1 细胞。PMS 阻止了 HG 引起的活性氧 (ROS) 和丙二醛 (MDA) 产生的增加以及超氧化物歧化酶 (SOD) 活性的降低。qRT-PCR 和 ELISA 测定证明了抗炎活性PMS，如 HG 诱导的 HBZY-1 细胞中 TNF-α、IL-1β 和 IL-6 水平降低所证明。此外，由 HG 引起的 HBZY-1 细胞中纤连蛋白 (FN) 和 IV 型胶原蛋白 (Col IV) 水平的增加也被 PMS 治疗降低。此外，PMS 显着抑制了 HG 诱导的 HBZY-1 细胞中 Akt/NF-κB 信号传导的激活。总之，这些发现表明 PMS 通过抑制氧化应激、炎症反应和细胞外基质 (ECM) 积累，从而减轻了 HG 诱导的 HBZY-1 细胞损伤。因此，PMS 可能具有治疗 DN 的潜在能力。这些发现表明 PMS 通过抑制氧化应激、炎症反应和细胞外基质 (ECM) 积累，从而减轻了 HG 诱导的 HBZY-1 细胞损伤。因此，PMS 可能具有治疗 DN 的潜在能力。这些发现表明 PMS 通过抑制氧化应激、炎症反应和细胞外基质 (ECM) 积累来减轻 HG 诱导的 HBZY-1 细胞损伤。因此，PMS 可能具有治疗 DN 的潜在能力。