Benign prostatic hyperplasia (BPH) is non-cancerous condition of enlargement of the prostate, a common occurrence in older men. The immature fruits of Poncirus trifoliata (L.) Rafinesque (Rutaceae), Ponciri Fructus are widely used in traditional oriental medicine for the therapy of various diseases. However, little is known about the mechanism underlying the pathogenesis of BPH. In the present study, we investigated the protective effects of a Ponciri Fructus extract (PFE) on the development of BPH in a in a rat model of BPH induced by testosterone propionate (TP). Male Sprague Dawley rats were used as a model of BPH after its induction by daily subcutaneous injections of TP/corn oil, for a period of four weeks. PFE was administrated daily 1 h before TP/corn oil injection by oral gavage at a dose level of 200 mg/kg during the 4 weeks of TP/corn oil injections. All rats were sacrificed at the end of the experiment, we measured the relative prostate weight, the levels of testosterone and dihydrotestosterone (DHT), histological changes, activities of antioxidant enzymes (catalase, glutathione peroxidase, glutathione reductase, and superoxide dismutase), and expression of proliferating cell nuclear antigen (PCNA). In addition, we also measured the inhibition (%) of 5α-reductase in the prostatic tissue. Our findings indicate that PFE significantly inhibited the development of BPH; decreased the relative prostate weight, the level of testosterone and DHT in serum and prostatic tissue, prostatic hyperplasia, expression of PCNA, and increased the antioxidant enzymes. Moreover, PFE showed a weak inhibitory activity on 5α-reductase. These results suggest that PFE may be used as a therapeutic agent for BPH via antiproliferative and antioxidant effects.

Atopic dermatitis (AD) is a prevalent chronic inflammatory skin disease. The use of immunomodulatory corticosteroids in AD treatment causes adverse side effects. Therefore, novel natural anti-inflammatory therapeutics are needed. The aim of the present study was to investigate the anti-allergic and anti-inflammatory activities of kuwanon G and morusin. To investigate the effect of kuwanon G and morusin on skin inflammation, enzyme-linked immunosorbent assays (ELISA) to quantitate secreted (RANTES/CCL5), thymus- and activation-regulated chemokine (TARC/CCL17), and macrophage-derived chemokine (MDC/CCL22) were performed, followed by Western blotting to measure the phosphorylation of signal transducer and activator of transcription 1 (STAT1) and nuclear transcription factor-κB (NF-κB) p65 in tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ)-stimulated HaCaT keratinocytes. In order to evaluate the anti-allergic effects, ELISA to quantify histamine and leukotriene C₄ (LTC₄) production and Western blotting to measure 5-lipoxygenase (5-LO) activation were performed using PMA and A23187-stimulated MC/9 mast cells. Kuwanon G reduced the release of RANTES/CCL5, TARC/CCL17, and MDC/CCL22 via down-regulation of STAT1 and NF-κB p65 signaling in TNF-α and IFN-γ-stimulated HaCaT keratinocytes. Kuwanon G also inhibited histamine production and 5-LO activation in PMA and A23187-stimulated MC/9 mast cells. Morusin inhibited RANTES/CCL5 and TARC/CCL17 secretion via the suppression of STAT1 and NF-κB p65 phosphorylation in TNF-α and IFN-γ-stimulated HaCaT keratinocytes, and the release of histamine and LTC₄ by suppressing 5-LO activation in PMA and A23187-stimulated MC/9 mast cells. Kuwanon G and morusin are potential anti-inflammatory mediators for the treatment of allergic and inflammatory skin diseases such as AD.

Curcuma aromaticais an herbal medicine and traditionally used for the treatment of various diseases in Asia. We investigated the effects ofC. aromaticawater extract (CAW) in the stomach of rats with ethanol-induced gastritis. Gastritis was induced in rats by intragastric administration of 5 mL/kg body weight of absolute ethanol. The CAW groups were given 250 or 500 mg of extract/kg 2 h before administration of ethanol, respectively. To determine the antioxidant effects of CAW, we determined the level of lipid peroxidation, the level of reduced glutathione (GSH), the activities of catalase, degree of inflammation, and mucus production in the stomach. CAW reduced ethanol-induced inflammation and loss of epithelial cells and increased the mucus production in the stomach. CAW reduced the increase in lipid peroxidation associated with ethanol-induced gastritis (250 and 500 mg/kg,p<0.01, resp.) and increased mucosal GSH content (500 mg/kg,p<0.01) and the activity of catalase (250 and 500 mg/kg,p<0.01, resp.). CAW increased the production of prostaglandin E₂. These findings suggest that CAW protects against ethanol-induced gastric mucosa injury by increasing antioxidant status. We suggest that CAW could be developed for the treatment of gastritis induced by alcohol.

Acetaminophen (N-acetyl-p-aminophenol, APAP) is a safe and effective analgesic at therapeutic dosage. However, APAP overdose is a major cause of acute liver injury. Gamisoyo-san (GMSYS; Jiaweixiaoyao-san in Chinese, Kamishoyo-san in Japanese), a traditional herbal formula, is used to treat phlegm and cough in Korea. The purpose of this study was to investigate the hepatoprotective effect of GMSYS against APAP-induced liver injury in vitro and in vivo. We evaluated the effect of GMSYS on APAP-induced hepatotoxicity by measuring cell viability in murine BNL CL.2 liver cells. Additionally, BALB/c mice were orally administered with GMSYS once daily for 7 days. Eighteen hours after the last administration, mice were intraperitoneally injected with 200 mg/kg APAP. Plasma alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels, hepatic antioxidants, and histological changes were examined. Pretreatment with GMSYS attenuated the decrease in cell viability induced by APAP in BNL CL.2 cells. In mice, pre-administration with GMSYS alleviated APAP-induced hepatotoxicity by decreasing plasma ALT and AST activities and hepatic malondialdehyde, and by increasing the total glutathione (GSH)/reduced GSH ratio and the activities of several antioxidants such as superoxide dismutase, catalase, GSH peroxidase, GSH reductase, GSH-S-transferase, and heme oxygenase-1. GMSYS has a protective effect against APAP-induced acute liver injury by decreasing plasma transaminases and increasing antioxidants. GMSYS may be an effective candidate for the prevention of acute liver injury.