Beijing Advanced Innovation Center for Food Nutrition and Human Health, Beijing Technology and Business University, Fucheng Road, Beijing, 100048, China.
Chemistry and Materials Engineering, Beijing Technology and Business University, 11 Fucheng Road, Haidian District, Beijing, 100048, China.
BMC Complement Med Ther. 2021 Jan 14;21(1):34. doi: 10.1186/s12906-020-03197-8.
Panax notoginseng is one of the most valuable traditional Chinese medicines. Polysaccharides in P. notoginseng has been shown to significantly reduce the incidence of human diseases. However the application of fermentation technology in Panax notoginseng is not common, and the mechanism of action of P. notoginseng polysaccharides produced by fermentation is still unclear. The specific biological mechanisms of fermented P. notoginseng polysaccharides (FPNP) suppresses HO-induced apoptosis in human dermal fibroblast (HDF) and the underlying mechanism are not well understood.
In this study, the effects of water extracted and fermentation on concentration of polysaccharides in P. notoginseng extracts were analyzed. After the HO-induced HDF model of oxidative damage was established, and then discussed by the expression of cell markers, including ROS, MDA, SOD, CAT, GSH-Px and MMP-1, COL-I, ELN, which were detected by related ELISA kits. The expression of TGF-β/Smad pathway markers were tested by qRT-PCR to determine whether FPNP exerted antioxidant activity through TGF-β signaling in HDF cells.
The polysaccharide content of Panax notoginseng increased after Saccharomyces cerevisiae CGMCC 17452 fermentation. In the FPNP treatment group, ROS and MDA contents were decreased, reversed the down-regulation of the antioxidant activity and expression of antioxidant enzyme (CAT, GSH-Px and SOD) induced by HO. Furthermore, the up-regulation in expression of TGF-β, Smad2/3 and the down-regulation in the expression of Smad7 in FPNP treated groups revealed that FPNP can inhibit HO-induced collagen and elastin injury by activating TGF-β/Smad signaling pathway.
It was shown that FPNP could inhibit the damage of collagen and elastin induced by HO by activating the TGF-β/Smad signaling pathway, thereby protecting against the oxidative damage induced by hydrogen peroxide. FPNP may be an effective attenuating healing agent that protects the skin from oxidative stress and wrinkles.
三七是最有价值的传统中药之一。研究表明，三七多糖可显著降低人类疾病的发病率。然而，发酵技术在三七中的应用并不常见，发酵产生的三七多糖的作用机制尚不清楚。发酵三七多糖（FPNP）抑制人真皮成纤维细胞（HDF）HO 诱导细胞凋亡的具体生物学机制以及潜在机制尚不清楚。
本研究分析了水提和发酵对三七提取物中多糖浓度的影响。在建立 HO 诱导的 HDF 氧化损伤模型后，通过相关 ELISA 试剂盒检测 ROS、MDA、SOD、CAT、GSH-Px 和 MMP-1、COL-I、ELN 等细胞标志物的表达，探讨其作用。通过 qRT-PCR 检测 TGF-β/Smad 通路标志物的表达，确定 FPNP 是否通过 TGF-β 信号通路在 HDF 细胞中发挥抗氧化活性。
经酿酒酵母 CGMCC 17452 发酵后，三七中多糖含量增加。在 FPNP 处理组中，ROS 和 MDA 含量降低，逆转了 HO 诱导的抗氧化活性和抗氧化酶（CAT、GSH-Px 和 SOD）表达下调。此外，FPNP 处理组 TGF-β、Smad2/3 表达上调，Smad7 表达下调，表明 FPNP 可通过激活 TGF-β/Smad 信号通路抑制 HO 诱导的胶原蛋白和弹性蛋白损伤。
结果表明，FPNP 可通过激活 TGF-β/Smad 信号通路抑制 HO 诱导的胶原蛋白和弹性蛋白损伤，从而保护过氧化氢诱导的氧化损伤。FPNP 可能是一种有效的皮肤抗氧化和抗皱修复剂。
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