Ocimum sanctum, Zingiber officinale, and Piper nigrum extracts and their effects on gut microbiota modulations (prebiotic potential), basal inflammatory markers and lipid levels: oral supplementation study in healthy rats.

CONTEXT: Ocimum sanctum Linn (Labiatae) (OS), Zingiber officinale Rose (Zingiberaceae) (ZO), and Piper nigrum Linn (Piperaceae) (PN) are used in traditional medicine as immunomodulator, anti-inflammatory, and bioavailability enhancer agents. OBJECTIVE: Active phytoconstituents of OS, ZO, PN hydro-alcoholic extracts and their effects on gut microbiota, basal inflammation and lipid profile were investigated in rats. MATERIALS AND METHODS: Active phytoconstituents of extracts were analysed using HPLC and GC-MS. SD rats were supplemented with individual/combined extracts (OS-850; ZO-500; PN-100 mg/kg Bw) and Fructooligosaccharide (standard prebiotic-5g/kg-Bw), orally for 30 days. Haematology, lipid profile, LPS, CRP, IL-6, insulin and histology of vital organs were analysed. Caecal bacterial levels were assessed by RT-PCR. RESULTS: High content of phenolic compounds luteolin-7-O-glucoside (430 ± 2.3 mg/100g), gallic acid (84.13 ± 1.2 mg/100 g) and flavones (88.18 ± 1.8 mg/100 g) were found in OS, ZO, and PN, respectively. Combined extract was rich in luteolin-7-O-glucoside (266.0 ± 1.80 mg/100 g). Essential oils including methyleugenol (13.96%), 6-shogaol (11.00%), piperine (18.26%), and cyclopentasiloxane (10.06%) were higher in OS, ZO, PN and combined extract. Higher levels of caecal Lactobacillus (1.7-3.4-fold), Bifidobacterium (5.89-28.4-fold), and lower levels of Firmicutes (0.04-0.91-fold), Bacteroides (0.69-0.88-fold) were noted among extracts and FOS supplemented rats. Significant (p < 0.05) decrease in plasma lipid profile and LPS was noted in all supplemented rats. DISCUSSION AND CONCLUSIONS: The current study could be first of its kind in exploring prebiotic potential of OS, ZO, PN and their effect on native gut bacterial population.

Erythrocyte Antioxidant Defenses Against Cigarette Smoking in Ischemic Heart Disease.

BACKGROUND: Cigarette smoke promotes atherogenesis by producing oxygen-derived free radicals. AIM: The present study was conducted to determine the effect of cigarette smoking on lipid peroxidation and erythrocyte antioxidant status in ischemic heart disease (IHD). MATERIALS AND METHODS: A total of 327 male subjects were enrolled for this study, divided into two groups consisting of 200 patients, who were consecutively admitted for IHD in the intensive cardiac care unit (ICCU) of a Government Hospital and 127 age matched male healthy subjects. Both the groups were subsequently categorised into smokers and non smokers sub groups depending upon the smoking history {>/= 20 pack years of smoking; (20 cigarettes per day for one year constitutes one pack year)}. All 327 subjects were investigated for lipid profile, malondialdehyde (MDA) levels and the antioxidant enzymes catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPX). STATISTICAL ANALYSIS: The differences in the parameters between the groups were tested for significance by one way ANOVA using the SPSS software version 19. A p-value of < 0.001 was considered to be significant statistically. Multiple comparisons were made between all the four groups by Post Hoc Tukey test. RESULTS: There was highly significant difference (p<0.001) observed in GPX activity, in comparison to CAT and SOD (p=0.032, p=0.009) between smokers vs non smokers in control group as well as patient group. The plasma MDA levels were found to be increased significantly (p<0.001) in IHD patients, who smoked as compared to those who did not. CONCLUSION: Chronic smoking enhances erythrocyte lipid peroxidation in IHD patients with concomitant failure of both plasma and erythrocyte antioxidant defense mechanisms. Along with conventional lipid markers and plasma MDA levels, the erythrocyte GPX activity was observed to be a better marker of oxidative stress, in chronic smokers, who are at risk of developing IHD.

Association of Angiotensin converting enzyme gene insertion / deletion polymorphism with risk of ischemic heart disease in a population of smokers in southern India.

BACKGROUND: Ischemic heart disease (IHD) remains a major public health problem nationally and internationally. Smoking is a major risk factor for IHD.The deletion (D) allele of the angiotensin converting enzyme (ACE) gene polymorphism has been associated with hypertension, ischemic stroke and myocardial infarction. The present study was carried out to determine the association of the ACE gene insertion/deletion (I/D) polymorphism in IHD patients with and without smoking. MATERIALS AND METHODS: One hundred seven male IHD patients admitted consecutively in the Cardiology unit of a Government Hospital and 100 age and sex matched healthy controls were enrolled in this study.The patients were further divided into smokers and nonsmokers. All the subjects were checked for I/D polymorphism of ACE gene, which is mapped to 17q23.3 with OMIM no 106180, by polymerase chain reaction (PCR). The subjects were also investigated for lipid profile and ejection fraction (EF). RESULTS: We found significant difference in the distribution of D allele between patients and controls (p=0.009, OR 1.69, 95% CI 1.139 to 2.517).The significantly lower EF (p<0.001) was suggestive of greater cardiovascular compromise in smokers. The frequency of ID genotype was significantly associated with cases compared to controls (p=0.012, OR 2.054, 95% CI 1.1694-3.624) but was not significantly associated with smokers as compared to nonsmokers. CONCLUSION: We infer significant association of D allele with IHD. The smokers with ID genotype should be put on prophylactic ACE inhibitor therapy to prevent the morbidity and mortality associated with IHD.