Combined Extracts of Artemisia and Green Tea, Mitigated Alcoholic Gastritis Via Enhanced Heat-shock Protein 27 / 대한소화기학회지

BACKGROUND/AIMS: Several lines of evidence from epidemiologic and laboratory studies have shown that the consumption of Artemisia or green tea extracts (MPGT) is inversely associated with the risk of alcohol-induced damage and other chronic diseases. Supported by previous studies showing that the combined extract of Artemisia and green tea, MPGT, exerted significantly either antioxidative or anti-inflammatory actions against Helicobacter pylori-associated gastric diseases, it was hypothesized that MPGT can offer protection against alcoholic gastritis. METHODS: Ethanol was administered to induce gastric damage in Wistar rats, which had been pretreated with various doses of MPGT, to measure the rescuing action of a MPGT pretreatment against ethanol-induced gastric damage. In addition, the molecular mechanisms for the preventive effects were examined. RESULTS: The MPGT pretreatment (100, 300, and 500 mg/kg) alleviated the ethanol-induced gastric damage, which was evidenced by the significant decrease in calcium-dependent phospholipase A2, MAPKs, and NF-κB levels compared to ethanol alone. Furthermore, the MPGT pretreatment preserved 15-prostaglandin dehydrogenase, whereas cyclooxygenase-2 was decreased significantly. All of these biochemical changes led to the significant alleviation of alcohol-associated gastric mucosal damage. Ethanol significantly increased the TUNEL positivity in the stomach, but MPGT decreased the apoptotic index significantly, which was associated with significantly lower pathological scores of ethanol-induced mucosal ulcerations. The significant protective changes observed alcoholic gastritis with MPGT were related to the increased expression of cytoprotective genes, such as heat-shock protein (HSP)27, HSP60, and PDGF. CONCLUSIONS: The efficient anti-inflammatory, anti-apoptotic, and regenerative actions of MPGT make it a potential nutrient phytoceutical to rescue the stomach from alcoholic gastritis.

Randomized, Double-blind, Placebo-controlled Clinical Trial for the Evaluation of the Efficacy and Safety of Artemisia and Green Tea Extract SD1003F in Volunteers with Helicobacter pylori-associated Gastric Discomfort

BACKGROUND/AIMS: A previous study showed that dietary intervention with Artemisia and green tea extracts, i.e., SD1003F, relieved Helicobacter pylori-associated chronic atrophic gastritis in a mouse model. We continue the research through the current randomized double-blind clinical trial to evaluate the efficacy and safety of the intervention for H. pylori-associated gastric discomfort. MATERIALS AND METHODS: Forty-nine volunteers who tested positive for H. pylori infection received either placebo or SD1003F for 10 weeks and their functional dyspepsia-related quality of life (QOL) was evaluated. H. pylori infection using a urea breath test (UBT), measurement of pepsinogen level using GastroPanel. Adverse effects with biochemical changes were also evaluated. RESULTS: SD1003F administration significantly improved health related-QOL, including dietary intake, emotional stability, life pattern, and social factors relevant to gastric discomfort, in comparison to the control (P < 0.05). The mean UBT measurement significantly decreased in the SD1003F group (P < 0.05). In 2 of the 24 volunteers, SD1003F alone eradicated H. pylori infection, with significant improvements in endoscopic findings. GastroPanel analysis revealed significant improvements that reflect rejuvenation of gastric atrophy in the SD1003F group. No significant side effect was observed in any participant. CONCLUSIONS: SD1003F (Artemisia and green tea extract), is a potential phytochemical to improve H. pylori-associated gastric discomfort.

Heme Oxygenase-1 Induction and Anti-inflammatory Actions of Atractylodes macrocephala and Taraxacum herba Extracts Prevented Colitis and Was More Effective than Sulfasalazine in Preventing Relapse

BACKGROUND/AIMS: In inflammatory bowel disease (IBD), repeated bouts of remission and relapse occur in patients and can impose a risk of colitis-associated cancer. We hypothesized that plant extracts of Atractylodes macrocephala (AM) or Taraxacum herba (TH) may be better than sulfasalazine for treating this disease because these extracts can promote additional regeneration. METHODS: Murine intestinal epithelial IEC-6 cells were pretreated with AM or TH before a lipopolysaccharide (LPS)-induced challenge. Acute colitis was induced with 7 days of dextran sulfate sodium (DSS) in male C57BL/6 mice, and extracts of AM and TH were administered for 2 weeks before DSS administration. RESULTS: In vitro studies demonstrated that AM or TH treatment reduced LPS-induced COX-2 and tumor necrosis factor-α mRNA levels but increased heme oxygenase-1 (HO-1). Oral preadministration of AM and TH rescued mice from DSS-induced colitis by inhibiting inflammatory mediators via inactivated extracellular signal regulated kinase and repressed nuclear factor κB and signal transducer and activator of transcription 3, but the effect was weaker for sulfasalazine than that for the extracts. Anti-inflammatory activities occurred via the inhibition of macrophage and T lymphocyte infiltrations. Unlike sulfasalazine, which did not induce HO-1, TH extracts afforded significant HO-1 induction. CONCLUSIONS: Because the AM or TH extracts were far superior in preventing DSS-induced colitis than sulfasalazine, AM or TH extracts can be considered natural agents that can prevent IBD relapse.

Helicobacter pylori Infection and Food Intervention for Preventing Associated Gastric Diseases Including Gastric Cancer

Since the discovery of Helicobacter pylori infection as the major cause of gastroduodenal disorders including acute and chronic gastritis, gastroduodenal ulcer, chronic atrophic gastritis, and gastric malignancy almost three decades ago, the possibility of preventing these clinical diseases through eradication has been the focus of active research and debate, especially since eradication can prevent cancer. Eradication intervenes with the initiation and progression of mucosal atrophy, metaplasia, dysplasia and gastric cancer. Our group hypothesized that nutritional interventions can rejuvenate the atrophic mucosa and ameliorate H. pylori-associated gastric inflammation. In this review article, the experience and outcomes regarding nutritional applications to rejuvenate gastric atrophy will be introduced. Korean red ginseng, garlic extracts, cancer preventive Korea Kimchi, n-3 polyunsaturated fatty acids, special form of licorice, and probiotics will be reviewed. The detailed effects of dietary and bacterial eradication therapy on disease progression and lesion reversibility are discussed.

Effect of Ginseng on Penile Erection: A combined in vitro and in vivo study / 대한남성과학회지

PURPOSE: Korean ginseng (KG) has been used as a general tonic in oriental society. The present study was undertaken to investigate the effect of total saponin (TS), a major extract of KG, and non-saponin components of KG on penile erection for evaluation of the possibility of developing KG as an pharmacological agent. MATERIALS AND METHODS: Strips of rabbit corpus cavernosum were mounted in organ chambers to measure isometric tension, with the treatment of TS and non-saponin components including methanol extracts, ethylacetate extract and H2O extract. We observed the relaxing effect of TS and non-saponin components, which were represented by % relaxation compared to 10-3M sodium nitroprusside-induced relaxation. In adult Sprague Dawley rats, we observed the increase of intracavernous pressure (delta ICP) and duration of tumescence (DT) by intracavernosal injection of TS. RESULTS: TS (1-4mg/cc) significantly relaxed the strips precontracted with phenylephrine (10(-5)M) in dose dependent manner (%relaxation: 5.8-36.7%). Intracavernous injections of TS (0.05mg-3.2mg/0.1cc) induced penile erection (delta ICP: 1.3-21.3mmHg, DT: 0.3-5.2min) in dose dependent manner. The cumulative additions of all non-saponin components at concentrations from 0.5mg/cc to 4mg/cc relaxed the strips in concentration-dependent manner. The maximal relaxing effect were 14.7% in methanol extract, 16.9% in H2O extract, 18.2% in ethylacetate extract. CONCLUSIONS: With the results, ginseng induces penile erection by relaxing corpus cavernosum and suggest that ginseng is not doing its action as a single component but ginseng is doing rather its action as complexes with saponin and non-saponin components.

Role of nitric oxide in penile erection

The present study was undertaken to investigate the role of nitric oxide (NO) in erectile physiology by correlating its action with the existence and activity of nitric oxide synthase (NOS), which produces NO. We applied Western blot analysis in both human and rat penile tissue. In the rat, reduced nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase staining and spectrophotometric assay were also performed, in addition to in vivo electroerection study with pharmacological manipulation. Western blot analysis identified a protein of 155 KDa identical to the neural form of NOS in the human and rat penis. The NOS blot densities in the two species were similar, and both were lower than that in the rat cerebellum. Histochemical staining localized NOS to neurons innervating the corpora cavernosa, including the pelvic plexus, the cavernosal nerves and their terminal fibers within the corporeal erectile tissue, and dorsal penile nerves. NOS activity was also found in the cerebellum, urethra, penis, and urinary bladder, in decreasing order of intensity. Intracavernous injections of NOS inhibitor (L-NOARG or L-NAME in concentrations from 10(-6) M to 10(-3) M suppressed electrostimulation-induced erection in a concentration-dependent manner. Subsequent intracavernous injection of L-Arginine (10(-2) M) partially restored the erection. The neural form of constitutive NOS in the corpora cavernosa synthesizes NO, which mediates penile erection. Determination of cavernosal NOS expression or activity may permit characterization of certain pathological conditions that cause impotence.