Cardioprotective effects of aqueous extract of Oxalis corniculata in experimental myocardial infarction

The present study evaluated the protective potential of aqueous extract of Oxalis corniculata (OCE) against isoproterenol (ISO) induced myocardial infarction in rats. Myocardial infarction in rats was induced by isoproterenol (200 mg/kg) at an interval of 24 h for 2 days. OCE was given to rats as pretreatment for 30 days orally using an intragastric tube. Isoproterenol caused a significant increase in the activity of cardiac injury marker enzymes like creatine phosphokinase (CPK) and lactate dehydrogenase (LDH) and increased the concentration of serum lipids. OCE pretreatment significantly reduced the concentration of CPK, LDH, serum total cholesterol, LDL cholesterol and triglycerides. OCE also reduced the activity of lipogenic enzyme, glucose-6-phosphate dehydrogenase in ISO administered rats. Oxidative stress produced by isoproterenol was significantly lowered by the administration of OCE which was evident from increased activities of antioxidant enzymes (catalase and superoxide dismutase) and reduced concentration of lipid peroxidation products (TBARS and conjugated dienes). Concentration of vitamin C, protein sulfhydryl groups and reduced glutathione (GSH) was also high in OCE pretreated rats. Histopathology of heart of ISO administered rat pretreated with OCE showed normal myocardium with very little evidence of inflammatory infiltration. Results of our in vitro findings also confirmed that OCE exhibits significant antioxidant and radical scavenging activity against DPPH, superoxide and nitric oxide radicals. These findings provided evidence that O. corniculata was found to be protecting the myocardium against ischemic insult and the protective effect could attribute to its antioxidative and antihyperlipidemic activities.     

Cannabinoid receptor-2 (CB2) agonist ameliorates colitis in IL-10(-/-) mice by attenuating the activation of T cells and promoting their apoptosis

Inflammatory bowel disease (IBD) is a chronic intestinal inflammation caused by hyperactivated effector immune cells that produce pro-inflammatory cytokines. Recent studies have shown that the cannabinoid system may play a critical role in mediating protection against intestinal inflammation. However, the effect of cannabinoid receptor induction after chronic colitis progression has not been investigated. Here, we investigate the effect of cannabinoid receptor-2 (CB2) agonist, JWH-133, after chronic colitis in IL-10^−/− mice. JWH-133 effectively attenuated the overall clinical score, and reversed colitis-associated pathogenesis and decrease in body weight in IL-10^−/− mice. After JWH-133 treatment, the percentage of CD4⁺ T cells, neutrophils, mast cells, natural killer (NK1.1) cells, and activated T cells declined in the intestinal lamina propria (LP) and mesenteric lymph nodes (MLN) of mice with chronic colitis. JWH-133 was also effective in ameliorating dextran sodium sulfate (DSS)-induced colitis. In this model, JWH-133 reduced the number and percentage of macrophages and IFN-γ expressing cells that were induced during colitis progression. Treatment with aminoalkylindole 6-iodo-pravadoline (AM630), a CB2 receptor antagonist, reversed the colitis protection provided by JWH-133 treatment. Also, activated T cells were found to undergo apoptosis following JWH-133 treatment both in-vivo and in-vitro. These findings suggest that JWH-133 mediates its effect through CB2 receptors, and ameliorates chronic colitis by inducing apoptosis in activated T cells, reducing the numbers of activated T cells, and suppressing induction of mast cells, NK cells, and neutrophils at sites of inflammation in the LP. These results support the idea that the CB2 receptor agonists may serve as a therapeutic modality against IBD.     

Population screening for abdominal aortic aneurysm: evaluating the evidence against screening criteria

Screening for abdominal aortic aneurysm (AAA) has been initiated in the United Kingdom and United States. Screening using abdominal ultrasound scans allows AAAs to be detected and electively repaired before rupture. There is currently no policy for AAA screening in New Zealand (NZ). We reviewed literature to assess current evidence for AAA screening against standard criteria used to evaluate population-based screening programmes. AAA rupture has high mortality, and people of Maori ethnicity are disproportionately affected. Abdominal ultrasound is a valid screening tool, and elective repair is an effective treatment. Screening reduces AAA-related mortality by about 40% in elderly men. However, the age and comorbidities of AAA patients means rupture risk has to be weighed against elective repair risk. Overtreatment is likely, given most individuals with AAA will not experience rupture in their lifetime. AAA screening appears to be cost-effective. It is unclear if the health system could support all the elements of a AAA screening pathway. AAA appears to be an appropriate condition for which to consider population screening. We recommend research into the prevalence of AAA in NZ, the comorbidity profile of individuals with AAA, drivers of high mortality among Maori, and acceptability of AAA screening to the New Zealand public.