Vitamin C modulates adrenaline-augmented gastric injury via cardiac troponin/creatine kinase pathway in Wistar rats.

Objectives: Vitamin C has anti-oxidant benefits in the gastrointestinal tract and heart. This study investigated the effect of vitamin C on some gastric parameters in myocardial injury in rats. Materials and Methods: Thirty Wistar rats were divided into five groups (n = 6). Group 1 was the control and Group 2 (ADR) received 1 mg/kg of adrenaline subcutaneously on days 13 and 14. Group 3 received vitamin C (200 mg/kg) orally for 14 days. Group 4 received adrenaline (1 mg/kg) on days 1 and 2 and vitamin C from days 1 to 14. Group 5 received vitamin C till day 14 and adrenaline on days 13 and 14. All animals were sacrificed after 2 hr of pyloric ligation. Gastric secretion parameters were assessed while a blood sample was obtained for biochemical analysis. Results: Gastric juice volume, total gastric acidity, pepsin activity, cardiac troponin 1, creatine kinase-MB, and lactate dehydrogenase levels increased (P<0.05) in ADR only group relative to the control. Pre- and post-vitamin C treatment reduced (P<0.05) these markers to near normal. However, treatment with vitamin C reduced (P<0.05) ulcer score, and increased (P<0.05) pepsin activity, mucus weight, and serum vitamin C levels when compared with the ADR-only group. Pre-treatment with vitamin C resulted in a marked decrease (P<0.05) in gastric juice volume, pepsin activity, and total gastric acidity compared with post-treatment in the adrenaline-induced injury group. Conclusion: Vitamin C pretreatment reduces excessive gastric secretions, ulcer scores, and attenuates cardio-inflammatory responses in adrenaline-augmented myocardial injury in rats.

Gongronema latifolium leaf extract protects against dexamethasone-induced myocardial cell injury via cardiac oxido-inflammatory molecules modulation.

The use of glucocorticoids in the treatment of inflammatory disorders can result in myocardial injury. This study was carried out to investigate the protective effects of ethanolic leaf extract of Gongronema latifolium (GL) in dexamethasone (DEX)-induced myocardial injury. Wistar rats were assigned to 4 groups (n = 6) namely, control, GL, DEX, and DEX+GL groups. DEX (35 µg/kg body weight) was administered subcutaneously to induce myocardial injury, while GL leaf extract (200 mg/kg body weight) was administered orally. Both agents were administered to their respective groups for 14 days. DEX (p < .05) decreased nitric oxide and increased angiotensin-converting enzyme activity compared with the control. Serum superoxide dismutase activity and bilirubin level were decreased (p < .05), while malondialdehyde level was increased (p < .05) in the DEX group. Serum liver enzymes, inflammatory biomarkers (C-reactive protein and interleukin-6), and cardiac injury biomarkers (creatinine kinase, cardiac troponin-T, and lactate dehydrogenase) were significantly (p < .05) increased in the DEX group relative to the control. Administration of GL leaf extract attenuated these changes significantly. The study therefore suggests that GL is beneficial in the treatment of myocardial injury via the downregulation of high serum concentration of cardiac biomarkers, oxidative stress markers, and inflammatory biomarkers released as a result of the insult caused by glucocorticoid administration. PRACTICAL APPLICATIONS: In this study, we demonstrated that prolonged use of dexamethasone resulted in myocardial cell injury via increased production of reactive oxygen species, inflammatory biomarkers, and inhibition of nitric oxide, a potent vasodilator. The leaves extract of Gongronema latifolium elicits the anti-inflammatory and cardioprotective potential as an efficient inhibitor of free radicals with good antioxidant properties. The study provides scientific evidence of the therapeutic ability of the extract of G. latifolium in the treatment of DEX-induced myocardial injury and could be a drug candidate for the treatment of myocardial injury and inflammation in humans.

Oxidant-induced disruption of vascular K+ channel function: Implications for diabetic vasculopathy.

Diabetes in humans a chronic metabolic disorder characterised by hyperglycaemia, it is associated with an increased risk of cardiovascular disease, disruptions to metabolism and vascular functions. It is also linked to oxidative stress and its complications. Its role in vascular dysfunctions is generally reported without detailed impact on the molecular mechanisms. Potassium ion channel (K+ channels) are key regulators of vascular tone, and as membrane proteins, are modifiable by oxidant stress associated with diabetes. This review manuscript examined the impact of oxidant stress on vascular K+ channel functions in diabetes, its implication in vascular complications and metabolic and cardiovascular diseases.

Cardioprotective Role of Theobroma cacao against Isoproterenol-Induced Acute Myocardial Injury.

BACKGROUND: Antioxidants are beneficial in myocardial infarction (MI). It is suggestive that Theobroma cacao (TC) with rich antioxidant properties can be of health benefits in myocardial injury. AIM: The study investigated the effect of Theobroma cacao on cardioprotection in isoproterenol-induced myocardial infarction in rats. MATERIAL AND METHODS: Male Wistar rats divided into four groups of 6 rats were used for the study. In group 1, 0.9% normal saline placebo was administered via oral gavage to the control. Group 2 was the MI induced group that was given 100 mg/kg body weight isoproterenol subcutaneously twice at an interval of 24 hours. Group 3 was administered TC for 2 weeks at 100 mg/kg bodyweight via the oral route. Group 4 was pretreated with TC (100 mg/kg) via oral route for 2 weeks, immediately followed by the administration of 100 mg/kg body weight isoproterenol subcutaneously twice at an interval of 24 hours. The rats were sacrificed using chloroform anesthesia, and blood samples collected via cardiac puncture. The serum was analyzed for troponin level, lactate dehydrogenase (LDH), and malondialdehyde (MDA) level. RESULTS: The serum troponin, LDH, and MDA levels were found to be significantly (p<0.01) increased in the MI group compared with the control. Pretreatment with TC before MI induction significantly (p<0.01) prevented increased serum troponin, LDH, and MDA levels when compared with the MI group. There was also a significant (p<0.01) decrease in MDA in the TC group compared with the control. CONCLUSION: These results suggest that Theobroma cacao protects against isoproterenol-induced myocardial injury, possibly by preventing oxidative stress and consequent lipid peroxidation.

Quercetin exerts preventive, ameliorative and prophylactic effects on cadmium chloride - induced oxidative stress in the uterus and ovaries of female Wistar rats.

This study examined the possible protective effect of quercetin(QE) on cadmium chloride (CdCl2) - induced reproductive toxicity in female rats. Cadmium (Cd) accumulated in the uterus and ovaries of rats, decreased antioxidants [superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione (GSH)], and raised the concentrations of malondialdehyde (MDA) and hydrogen peroxide (H2O2) in the uterus and ovaries of rats. Serum concentrations of estradiol, progesterone, follicle stimulating hormone and luteinizing hormone decreased significantly after CdCl2 administration. Caspase-3 activity significantly increased in the ovaries, with an increase in Bax and a decrease in Bcl-2 protein expressions after CdCl2 treatment. Histopathology of the ovaries revealed significant decrease in follicle number, while the uterus showed cyst-like endometrial glands. All three models of QE treatment [pre-treatment (QE + CdCl2), post-treatment (CdCl2+QE), simultaneous treatment (CdCl2/QE)] decreased Cd accumulation, MDA, H2O2, and increased SOD, CAT and GPx activities in the uterus and ovaries, decreased apoptosis of follicular cells, and increased serum reproductive hormones. However, the QE pre-treated model offered better protection against CdCl2 relative to the other two models. These results suggest that, QE exerts multi-mechanistic protective effects against cadmium toxicity attributable to its antioxidant and anti-apoptotic actions.