Panaxydol, a C17-polyacetylene from Panax ginseng roots, exhibits cytotoxic and antimicrobial activities [1]. Panaxydol increased albumin secretion and alkaline phosphatase activity, and correspondingly decreased alpha-fetoprotein (AFP) secretion, as well as decreased the expression of Id1 regulator and increased the protein levels of p21 and p-ERK1/2 in liver carcinoma cell lines[2]. Panaxydol has been widely used to induce cancer cell death and promote Caspase-3 activation and PKCδ cleavage[3].
In vitro, Panaxydol treatment for 48 hours significantly inhibited the proliferation of rat C6 glioma cells, with an IC50 value of 39.5µM[4]. 10µM of Panaxydol incubation for 24 hours protected Schwann cells from hypoxia-induced cell death and increased the mRNA levels of neurotrophic factors NGF and BDNF[5]. Treatment with 50μg/ml Panaxydol for 2 hours significantly induced apoptosis in MCF-7 and Jurkat cells, promoting the release of mitochondrial cytochrome c and resulting in the loss of mitochondrial membrane potential[6].
In vivo, Panaxydol treatment via oral administration at a dose of 20mg/kg/day for 20 days significantly alleviated the kidney damage induced by aristolochic acid in rats, improved renal function, and promoted the expression levels of Nrf2, NQO1 and HO-1[7]. Continuous intraperitoneal injection of 20mg/kg dose of Panaxydol for three consecutive days significantly inhibited lipopolysaccharide (LPS)-induced acute lung injury (ALI) and ferroptosis in mice[8].
References:
[1] Knispel N, Ostrozhenkova E, Schramek N, et al. Biosynthesis of panaxynol and panaxydol in Panax ginseng[J]. Molecules, 2013, 18(7): 7686-7698.
[2] Wang Z J, Song L, Guo L C, et al. Induction of differentiation by panaxydol in human hepatocarcinoma SMMC-7721 cells via cAMP and MAP kinase dependent mechanism[J]. Yakugaku Zasshi, 2011, 131(6): 993-1000.
[3] Yan Z, Yang R, Jiang Y, et al. Induction of apoptosis in human promyelocytic leukemia HL60 cells by panaxynol and panaxydol[J]. Molecules, 2011, 16(7): 5561-5573.
[4] Hai J, Lin Q, Lu Y, et al. Growth inhibition and induction of differentiation by panaxydol in rat C6 glioma cells[J]. Neurological research, 2008, 30(1): 99-105.
[5] Zhu H, Wang W J, Ding W L, et al. Effect of panaxydol on hypoxia-induced cell death and expression and secretion of neurotrophic factors (NTFs) in hypoxic primary cultured Schwann cells[J]. Chemico-biological interactions, 2008, 174(1): 44-50.
[6] Kim J Y, Yu S J, Oh H J, et al. Panaxydol induces apoptosis through an increased intracellular calcium level, activation of JNK and p38 MAPK and NADPH oxidase-dependent generation of reactive oxygen species[J]. Apoptosis, 2011, 16(4): 347-358.
[7] Guo Y, Hu M, Ma J, et al. Protective effect of panaxydol against repeated administration of aristolochic acid on renal function and lipid peroxidation products via activating Keap1‐Nrf2/ARE pathway in rat kidney[J]. Journal of Biochemical and Molecular Toxicology, 2021, 35(1): e22619.
[8] Li J, Lu K, Sun F, et al. Panaxydol attenuates ferroptosis against LPS-induced acute lung injury in mice by Keap1-Nrf2/HO-1 pathway[J]. Journal of Translational Medicine, 2021, 19(1): 96.
Panaxydol是从人参根中提取的一种C17-多炔醇类化合物，具有细胞毒性和抗微生物活性[1]。Panaxydol能够增加白蛋白分泌和碱性磷酸酶活性，相应地降低甲胎蛋白（AFP）分泌，同时降低肝癌细胞系中Id1调节因子的表达，提高p21和p-ERK1/2的蛋白水平[2]。Panaxydol已被广泛用于诱导癌细胞死亡，并促进Caspase-3激活和PKCδ裂解[3]。
在体外，Panaxydol处理48小时显著抑制了大鼠C6胶质瘤细胞的增殖，IC50值为39.5µM[4]。使用10µM的Panaxydol孵育24小时，保护了雪旺细胞免受缺氧诱导的细胞死亡，并增加了神经营养因子NGF和BDNF的mRNA水平[5]。使用50µg/ml的Panaxydol处理2小时，显著诱导了MCF-7和Jurkat细胞凋亡，促进了线粒体细胞色素c的释放，并导致线粒体膜电位丧失 [6]。
在体内，每日口服20mg/kg剂量的Panaxydol，连续20天，显著减轻了马兜铃酸诱导的大鼠肾损伤，改善了肾功能，并促进了Nrf2、NQO1和HO-1的表达水平[7]。连续三天腹腔注射20mg/kg剂量的Panaxydol，显著抑制了脂多糖（LPS）诱导的小鼠急性肺损伤（ALI）和铁死亡[8]。