Our data demonstrate that H pylori infection promotes gastric epithelial cells invasion by activating MMP-9 and VEGF expression. These effects appear to be mediated through a NF-kappaB and COX-2 mediated pathway, as COX-2 or NF-kappaB inhibitor significantly attenuate the invasiveness of gastric cancer cells and the expressions of MMP-9 and VEGF protein.
Diabetic nephropathy progressed to end-stage renal disease (ESRD) is found in type 1 or type 2 diabetes. Oxidative stress is one of the precipitation factors in diabetic nephropathy. Previously, Hibiscus sabdariffa Linnaeus and its polyphenol extracts were found to possess antioxidative effects. This study is aimed to investigate the effect of Hibiscus sabdariffa L. polyphenol extract (HPE) in streptozotocin (STZ) induced diabetic nephropathy. The results show that HPE reduced kidney mass induced by STZ significantly, as well as improving hydropic change of renal proximal convoluted tubules in the rats. HPE also significantly reduced serum triglyceride, total cholesterol and LDL in STZ induced rats. Treatment with HPE significantly increased the activity of catalase and glutathione and reduced lipid peroxidation (thiobarbituric acid-reactive substances, TBARS). The findings of this research show the beneficial effects of HPE on STZ induced diabetic nephropathy including pathology, serum lipid profile and oxidative marker in kidney.
Chemopreventive agents are compounds that inhibit carcinogenesis when administered prior or subsequent to a course of carcinogen administration. The effects of dietary administration of crocin dyes on the hepatic damage induced by aflatoxin B1 (AFB1) and dimethylnitrosamine (DMN) in rats were investigated. Female Sprague-Dawley rats were treated with different dosages of AFB1 (0.9 or 4.5 mg/kg) or DMN (8 or 20 mg/kg) by i.p. administration, and the different degrees of hepatic damage were revealed by the elevations of levels of serum marker enzymes such as aspartate amino-transferase, alanine aminotransferase, alkaline phosphatase, gamma-glutamyl transpeptidase and lactic dehydrogenase. Pre-treatment of the animals with crocin dyes 50 mg/kg daily for three consecutive days, the enzyme elevations were significantly suppressed. This suggested that the crocin dyes possessed chemopreventive effects on the early acute hepatic damage induced by AFB1 or DMN. Feeding experiments demonstrated that crocin dyes at 0.1% in the diet could suppress partially the chronic hepatic damage induced by multiple dosages of AFB1 or DMN, but at a higher concentration of 1% crocin dye failed to do so because of their host toxicity. Crocin dyes are extracted from the fruits of Gardenia jasminoides and consist of carotenoids and geniposides as active principles. The protective mechanisms of crocin dyes may be attributed to their carotenoids which are converted metabolically to retinoids in rats.
Exposure to environmental tobacco smoke has been epidemiologically linked to heart disease among nonsmokers. However, the molecular mechanism behind the pathogenesis of cardiac disease is unknown. In this study, we found that Wistar rats, exposed to tobacco cigarette smoke at doses of 5, 10, or 15 cigarettes for 30 min twice a day for 1 month, had a dose-dependently reduced heart weight to body weight ratio and enhanced interstitial fibrosis as identified by histopathologic analysis. The mRNA and activity of matrix metalloprotease-2 (MMP-2), representing the progress of cardiac remodeling, were also elevated in the heart. In addition, we used reverse-transcriptase polymerase chain reaction and Western blotting to demonstrate significantly increased levels of the apoptotic effecter caspase-3 in treated animal hearts. Dose-dependently elevated mRNA and protein levels of Fas, and promoted apoptotic initiator caspase-8 (active form), a molecule of a death-receptor–dependent pathway, coupled with unaltered or decreased levels of cytosolic cytochrome c and the apoptotic initiator caspase-9 (active form), molecules of mitochondria-dependent pathways, may be indicative of cardiac apoptosis, which is Fas death-receptor apoptotic-signaling dependent, but not mitochondria pathway dependent in rats exposed to second-hand smoke (SHS). With regard to the regulation of survival pathway, using dot blotting, we found cardiac insulin-like growth factor-1 (IGF-1) and IGF-1 receptor mRNA levels to be significantly increased, indicating that compensative effects of IGF-1 survival signaling could occur. In conclusion, we found that the effects of SHS on cardiomyocyte are mediated by the Fas death-receptor–dependent apoptotic pathway and might be related to the epidemiologic incidence of cardiac disease of SHS-exposed non-smokers.
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