Abstract
Polyacetylenic compounds isolated from Panax species are comprised of non-polar C17 compounds, exhibiting anti-inflammatory, antitumor, and antifungal activities. Panaxynol represents the major component of the essential oils of ginseng. We investigated whether panaxynol isolated from Panax vietnamensis (Vietnamese ginseng, VG) could prevent cisplatin-induced renal damage induced in vitro and in vivo. Cisplatin-induced apoptotic cell death was observed by staining with annexin V conjugated with Alexa Fluor 488, and western blotting evaluated the molecular mechanism. Panaxynol at concentrations above 0.25 μM prevented cisplatin-induced LLC-PK1 porcine renal proximal tubular cell death. LLC-PK1 cells treated with cisplatin demonstrated an increase in apoptotic cell death, whereas pretreatment with 2 and 4 μM panaxynol decreased this effect. Cisplatin demonstrated a marked increase in the phosphorylation of c-Jun N-terminal kinase (JNK), P38, and cleaved caspase-3. However, pretreatment with 2 and 4 μM panaxynol reversed the upregulated phosphorylation of JNK, P38, and the expression of cleaved caspase-3. We confirmed that the protective effect of panaxynol isolated from P. vietnamensis in LLC-PK1 cells was at least partially mediated by reducing the cisplatin-induced apoptotic damage. In the animal study, panaxynol treatment ameliorated body weight loss and blood renal function markers and downregulated the mRNA expression of inflammatory mediators.
Highlights
The kidney is the main organ responsible for maintaining homeostasis in the body by regulating the volume and chemical composition of body fluids [1]
Protective Effect of Panaxynol Isolated from Panax vietnamensis on Cisplatin-Induced LLC-PK1 Cell Death
To evaluate the protective effect of panaxynol (Figure 2A), LLC-PK1 cells were exposed to 25 μM cisplatin in the presence or absence of panaxynol for 24 h
Summary
The kidney is the main organ responsible for maintaining homeostasis in the body by regulating the volume and chemical composition of body fluids [1]. Biomolecules 2019, 9, 890 new cases and 9.6 million cancer deaths in 2018 [4]. This necessitates the discovery of alternatives that are effective but less toxic in cancer patients [5]. Several studies have reported the protective effects of ginsenoside in damaged proximal tubular cells, a major site for cisplatin effects, and in animal models of cisplatin-induced renal damage [6]. In human embryonic kidney epithelial cells (HEK293) and mice, ginsenoside Rb3 reduced renal damage via the regulation of autophagy and inhibition of proximal tubular apoptosis [7]. Ginsenosides Rh2, Re, and Rg5 prevent oxidative stress, inflammation, and apoptosis in cisplatin-induced renal damage in mice [8,9,10]
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