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Aims: This study was carried out to evaluate the hepatoprotective effect of Platycodon grandiflorum (PG) in ethanol (EtOH)-induced liver damage. Methods and Results: PG treatment (both the total extract and saponin fraction) significantly blocked EtOH-induced oxidative stress through the preservation of activities of antioxidant enzymes in HepG2 cells. Furthermore, while the administration of EtOH to C57BL/6 mice for 6 weeks induced liver damage, along with a significant increase in plasma glutamic oxalacetic transaminase, glutamic pyruvic transaminase, hepatic triglyceride and thiobarbituric acid reactive substance levels, PG treatment significantly decreased glutamic oxalacetic transaminase, glutamic pyruvic transaminase, hepatic triglyceride and thiobarbituric acid reactive substance levels compared with the EtOH-treated control group (p < 0.05). Histological observation by hematoxylin-eosin and oil red O staining in the liver showed more effective inhibition of lipid accumulation in PG-treated groups, as compared to the EtOH-treated control group. Additionally, PG treatments appeared to enhance the activities of superoxide dismutase and catalase in the liver (p < 0.05). Conclusion: These results suggest that PG has a protective effect against EtOH-induced oxidative damage, possibly by inhibition of lipid accumulation and peroxidation through the enhancement of the antioxidant defense system. PG might be useful as a therapeutically potent natural ingredient for the prevention of chronic EtOH-induced oxidative stress and liver damage.

This study evaluated the anti-obesity effects of Phellinus baumii extract (PBE) in high-fat diet (HFD)-fed mice. Male 8-week-old C57BL/6 mice were randomly divided into four groups: control, normal chow diet plus vehicle; HFD-control, high-fat plus vehicle; HFD plus orlistat (Xenical(®), Roche, Basel, Switzerland) (50 mg/kg); and HFD plus PBE (500 mg/kg). PBE was administered daily by oral gavage for 12 weeks. Oral administration of PBE (500 mg/kg) significantly reduced body weight gain, hepatic lipid concentrations, and fat accumulation in epididymal adipocytes compared with mice fed HFD alone (P < .05). mRNA expression of genes related to triglyceride (TG) synthesis was suppressed in the PBE groups, and fatty acid synthase activity was also significantly inhibited (P < .05). Furthermore, we evaluated the effect of PBE on TG absorption and detected marked reduction in TG absorption in Xenical- and PBE-treated mice compared with the control group (P < .05). To determine the active compound of PBE, fractionation was conducted, and interfungin A, davallialactone, and hypholomine B were identified as the main compounds. Among the three identified compounds, as a representative compound, davallialactone was also shown to suppress fat accumulation in an in vitro model system. These anti-obesity and hypolipidemic effects appear to be partly mediated by suppressing plasma and hepatic fat accumulation through the inhibition of enzymes associated with hepatic and intestinal lipid absorption and synthesis.

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Melicope ptelefolia has been traditionally used to treat rheumatism and fever. The present study aimed to investigate the therapeutic effect of 3,5-di-C-β-d-glucopyranosyl phloroacetophenone (βGP), a main component of M. ptelefolia, on rheumatoid arthritis (RA). A model of collagen-induced arthritis (CIA) was established in mice using the RAW 264.7 murine macrophage cell line and mouse embryonic fibroblasts (MEFs). The clinical scores of arthritis, swelling, histopathological findings, and micro-computed tomography in CIA mouse paws were assessed. The levels of anti-type II collagen antibody and cytokines were determined in the plasma and cell culture supernatant, respectively. Protein and gene expression levels were analyzed by western blot and reverse transcription-quantitative polymerase chain reaction analyses. βGP significantly decreased the gross arthritic scores of CIA mice and joint swelling, and decreased articular inflammation, cartilage degradation and bone erosion. However, βGP did not exert any effect on anti-type II collagen immunoglobulin G plasma levels or inflammatory cytokine expression in macrophages. βGP significantly suppressed the expression of interleukin-6 and leukemia inhibitory factor and decreased the phosphorylation of signal transducer and activator of transcription 3, and expression of receptor activator of nuclear factor-κB ligand in tumor necrosis factor-α-stimulated MEFs and in CIA mouse paws. Osteoclast-related gene expression was significantly reduced in CIA mouse paws. Taken together, βGP suppressed the development of RA by regulating the activation of synovial fibroblasts.