Co-Existent Hypertension with Diabetes Mellitus Exacerbates Renal Dysfunctions

Hypertension as well as diabetes mellitus has been reported to be a major risk factor for deteriorating kidney functions. However, there is paucity of reports on renal functions in a co-existence of hypertension and diabetic condition, hence, this study evaluates renal functions in hypertensive and diabetic co-morbidity. Participants were categorised into healthy, hypertension, diabetes and hypertension with diabetes group. Blood pressure was measured as well as fasting blood glucose and blood samples were collected from each participant to assay renal function indices. The results showed that there was substantial uraemia as well as a significant reduction glomerular filtration rate in co-morbid hypertension and diabetic patients. Fasting blood glucose and mean arterial blood pressure were considerably elevated while creatinine concentration was not significantly altered in comorbid hypertension and diabetic patients. This study revealed that co-existence of hypertension and diabetes mellitus exacerbated renal dysfunction comparatively to hypertension and diabetes mellitus

Possible mechanisms involved in the protective effect of lutein against cyclosporine-induced testicular damage in rats

Oxidative stress and aberrant inflammatory response have important implications in cyclosporin-induced reproductive functions. Previous studies have shown that agents with antioxidant and anti-inflammatory activities might be beneficial in reversing cyclosporin-induced reproductive impairment. Lutein is a naturally occurring compound with antioxidant and anti-inflammatory properties. However, the effect of lutein against cyclosporin-induced reproductive impairment remains in complete. Hence, we investigated the protective effect of lutein, specifically focusing on the role of nuclear factor erythroid 2 related factor-2 (Nrf2)/heme-oxygenase-1 (HO-1)/connexin-43 (Cx-43) upregulation system against cyclosporine-induced reproductive impairment. Six male Wistar rats were allotted into 5 groups and given daily gavage of cyclosporine (40 mg/kg) and/or lutein (30 mg/kg) for four (4) weeks or in combination, respectively. The testicular antioxidant scaffolds: superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH), add to sulfhydryl (T-SH), non-protein sulfhydryl (NP-SH), glutathione reductase (GR), glutathione-S -transferase (GST), glutathione peroxidase (GSH-Px), thiobarbituric acid reactive substances (TBARS), myeloperoxidase (MPO), testicular proinflammatory cytokines, apoptotic related protein, nucleic acids, sialic acid, testicular proton pump ATPase, stress responsive protein, BTB-related protein and total protein levels in the testes were assayed thereafter. Cyclosporin significantly increased NOX-1, TNF-α, IL-1β, MPO, caspase-3 and -9 levels, which were reversed by lutein. Lutein reversed cyclosporin-induced decreases in Nrf2, HO-1, BCL-2, cytochrome C, with corresponding increase in CAT, SOD, GSH, T-SH, NP-SH, GST, GR, GSH-Px, and Cx-43 levels compared to cyclosporin groups. Lutein also abates cyclosporin-induced alterations Na + -K + -ATPase activities. Our findings showed that lutein's protective effect against cyclosporin-induced reproductive impairment might be associated with mechanisms linked to its antioxidant, anti-apoptotic, and anti-inflammatory properties, notably through up-regulation of Nrf2/HO-1/Cx-43 signaling and down-regulation of NOX-1 signaling

The Role of Medicinal Plants in Diabetes Mellitus and Oxidative Stress: A Review

Diabetes mellitus is an endocrinology disorder of great global concern. It results from an irregularity in the secretion or action of insulin. It is a metabolic condition characterized by chronic hyperglycemia. Oxidative stress plays a critical role in the pathophysiology of some diseases such as diabetes, aging, cancer, cardiovascular disease, as well as liver and lung diseases. Oxidative stress occurs due to an imbalance between radical generation and radical scavenging. One of the main mechanisms for the development of diabetes complications is via oxidative stress. Oxidative stress is a main upstream occurrence for diabetes complications as well as the development of insulin resistivity. Medicinal plants can be useful in the treatment of numerous diseases and some of their healthful effects are due to their antioxidant activity. Their antihyperglycemic effect is very much linked to their antioxidant potential. This review summarized the antidiabetic potential of some medicinal plants in animal models. There is a continuous need to explore the medicinal capability of herbal products with antioxidant effects in the management of diabetes mellitus

Enhancements of Bcl-2/mTOR/ERK1/2 activities by antioxidant mechanisms confer cardioprotection on Ginkgo biloba supplement against isoprenaline-induced myocardial infarction in rats

Background: Myocyte necrosis and apoptosis can be severely induced by acute adrenergic stimulation due to the activation of several cell signalling pathways. However, uncertainty exists regarding the potential cardioprotective effects of Ginkgo biloba (GBS), a Chinese herbal supplement rich with antioxidants, on isoprenaline (ISO)-induced myocardial infarction. Therefore, this work was designed to investigate the cardioprotective mechanisms of GBS on ISO-induced myocardial infarction. Methods: Animals were selected into four groups. Groups 1 and 2 were pre-treated with normal saline (10 mL/kg i.p) for 28 days. Groups 3 and 4 received GBS (50 mg/kg, i.p) for 28 days. However, groups 2 and 4 were administered ISO (150 mg/kg, s.c) on days 27 and 28 respectively. Following the end of 28-day experiment, animals were euthanised and serum as well as heart tissue were harvested and processed for biochemical and histological examinations. Results: Our results showed that ISO induced cardiac necrosis, evidenced by increased levels of cardiac injury enzymes (LDH, GGT, CK-MB and cT-1), oxidative stress markers such as GSH, SOD, and CAT levels were significantly reduced while MDA and nitrite concntration were significantly increased. Inflammatory cytokines (IL-6 and TNF-α) were significantly increased while decreasing Bcl-2, mTOR and ERK1/2 cardiac immuno-expressions. Moreso, histological investigation revealed degeneration of cardiomyofibres together with patchy necrosis. However, pre-treatment with GBS significantly inhibited apoptotic processes evidenced by increased antioxidant-mediated activation of Bcl-2, mTOR and ERK1/2. GBS also suppressed the release of cardiac injury enzymes and histological changes were significantly improved. Conclusion: GBS protects myocardium against ISO-induced infarction by mechanisms related to antioxidant-mediated by enhancement of Bcl-2/mTOR/ERK1/2 activities

Chronic intermittent oxygen deprivation alters hippocampal cholinergic and glutamatergic system via oxido-inflammatory burden and HIF-1a/Bcl-2 activity in hypothyroid mice: Ameliorative role of Ginkgo biloba supplement

Background: Several investigations in recent years have reported a relationship between hypothyroidism or ischemia and central nervous system (CNS) beginning from fetal to adult life, but the effect of ischemia and hypothyroidism comorbidity on CNS and whether phytotherapeutic approach would attenuate this pathology remains unknown. Thus, the study investigated the role of ginkgo biloba supplement (GBS), a potent anti-oxido-inflammatory and neurorestorative plant-based product on hypoxic stress-induced neurobehavioral and neurophysiological alterations in hypothyroid mice, and the underpinning molecular mechanisms Methodology: Mice were orally pre-treated with Carbimazole (1.2 mg/kg) for 14 days to develop hypothyroidism. Post-hypothyroid induction, mice were treated orally with GBS (20 mg/kg) and levothyroxine (10 µg/kg) 1 hr before 20 min exposure to hypoxia (5 times daily) for 14 consecutive days. Symptoms of behavioral deficit and neuropsychiatry were evaluated in using different models. Thereafter, brain hippocampi were sectioned for biochemical assays, immunohistochemistry and histoarchitectural studies. Results: Herein, treatment with GBS suppressed spatial memory deficit and neuropsychiatric phenotypes and attenuated hippocampal cholinergic excitotoxicity by enhancing acetylcholinesterase enzyme and glutamatergic release in the hypothyroid mice following hypoxic stress exposure. The hippocampal endogenous antioxidant system was also upregulated with concomitant downregulation of inflammatory mediators. GBS treatment consequently regulated the hypothalamic-pituitary-adrenal axis to reduce corticosterone release. Additionally, our data showed that the suppressive impact of GBS on oxido-inflammatory mainstream decreases immunoexpression of hypoxic inducible factor-1alpha (HIF-1α) and loss of hippocampal pyramidal neurons in the CA3 region with marked increase in viable neuronal cells and upregulated immunoexpression of B-cell lymphoma-2 (Bcl-2) anti-apoptotic marker. Conclusion: Herein, we deduced that prolonged intermittent exposure to hypoxia in hypothyroidism may provoke further the psychological and physiological status in the hippocampal brain region. Meanwhile, reversal of these provocative effects by the GBS treatment might be playing an important effect to suppress the hypoxic/ischemic triggered neurobehavioral and neurophysiological alterations