BackgroundThough herbal medicines have been used for cancer prevention and treatment, their scientific evidences still remain unclear so far. Thus, complementary and alternative medicine (CAM) project has been actively executed to reveal the scientific evidences in the USA and other countries. In the present study, we elucidated antitumor mechanism of Chijongdan, an oriental prescription of Rhus verniciflua, processed Panax ginseng, Persicaria tinctoria and Realgar, that has been traditionally applied for cancer treatment in Korea.MethodsChijongdan was prepared with extracts of Rhus verniciflua, processed Panax ginseng, Persicaria tinctoria and processed Realgar. The cytotoxicity of Chijongdan was measured by MTT colorimetric assay. Cell cycle analysis was performed by FACS. Western blot was performed to see the apoptosis related proteins.ResultsChijongdan significantly exerted cytotoxicity in A549, H460 and H1299 non-small cell lung carcinoma (NSCLC) cells by MTT assay and also increased the number of ethidium homodimer positively stained cells in A549 NSCLC cells. Also, cell cycle analysis showed that Chijongdan increased sub-G1 population in a concentration dependent manner in A549 cells. In addition, Western blotting revealed that Chijongdan activated cleaved PARP, and caspase 9/3, while attenuated the expression of survival genes such as Bcl-2, Bcl-XL and survivin in A549 cells. Furthermore, Chijongdan suppressed the expression of ribosomal biogenesis related proteins such as upstream binding factor (UBF), Fibrillarin, NPM (B23) and Importin-7 (IPO7) and conversely pan-caspase inhibitor Z--VAD-FMK reversed the apoptotic ability of Chijongdan to cleave PARP and caspase 3 and attenuate the expression of UBF and Fibrillarin in A549 cells.ConclusionsThese findings suggest that Chijongdan induces apoptosis and inhibits ribosomal biogenesis proteins via caspase activation.
The bark of Rhus verniciflua Stokes (RVS) is used as a food additive and herbal medicine for various inflammatory disorders and cancer in Eastern Asia. RVS has been shown to exert anti-inflammatory effects in lipopolysaccharide (LPS)-stimulated macrophages in vitro, but whether oral administration of RVS affects the inflammatory response of macrophage needs to be verified. RVS was given orally to mice for ten days. For isolation of macrophages, intraperitoneal injection of thioglycollate was performed. For determination of serum inflammatory response, intraperitoneal injection of LPS was applied. RVS stimulated monocyte differentiation in thioglycollate-induced peritonitis by increasing the population of cells expressing CD11b and class A scavenger receptors. These monocyte-derived macrophages showed an increased uptake of acetylated low-density lipoprotein. When peritoneal macrophages from the RVS group were stimulated with LPS, the levels of tumor necrosis factor (TNF)-α and interleukin (IL)-6 in the supernatant decreased, but the level of IL-12 increased. The surface expression of CD86 was reduced, but surface expression of class II major histocompatibility complex molecules was increased. RVS suppressed the serum levels of LPS-induced TNF-α and IL-6. Collectively, RVS promoted monocyte differentiation upon inflammatory insults and conferred selective anti-inflammatory activity without causing overall inhibitory effects on immune cells.
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