Vanillylacetone attenuates cadmium chloride-induced hippocampal damage and memory loss through up-regulation of nuclear factor erythroid 2-related factor 2 gene and protein expression.

JOURNAL/nrgr/04.03/01300535-202412000-00030/figure1/v/2024-04-08T165401Z/r/image-tiff Memory loss and dementia are major public health concerns with a substantial economic burden. Oxidative stress has been shown to play a crucial role in the pathophysiology of hippocampal damage-induced memory impairment.

Metformin ameliorates ROS-p53-collagen axis of fibrosis and dyslipidemia in type 2 diabetes mellitus-induced left ventricular injury.

Background: The link between oxidative stress (ROS), apoptosis (p53) and fibrosis (collagen) in type 2 diabetes mellitus (T2DM)-induced cardiac injury in the presence and absence of the antidiabetic drug, metformin has not been investigated before.

Material And Methods: T2DM was induced in rats by a combination of high carbohydrate and fat diets (HCFD) and streptozotocin (50 mg/kg) injection. The protection group started metformin (200 mg/kg) treatment 14 days prior to the induction of diabetes and continued on metformin and HCFD until being sacrificed at week 12.

Suppression of type 2 diabetes mellitus-induced aortic ultrastructural alterations in rats by insulin: an association of vascular injury biomarkers.

Diabetes represents a major public health problem and an estimated 70% of people with diabetes die of cardiovascular complications. The protective effect of insulin treatment against ultrastructural damage to the tunica intima and tunica media of the aorta induced by type 2 diabetes mellitus (T2DM) has not been investigated before using transmission electron microscopy (TEM). Therefore, we induced T2DM in rats using high fat diet and streptozotocin (50 mg/kg) and administered insulin daily by i.

Minocycline protects against acrylamide-induced neurotoxicity and testicular damage in Sprague-Dawley rats.

This study investigated the protective effects of minocycline against acrylamide (ACR)-induced neurotoxicity and testicular damage in Sprague-Dawley rats. Forty rats were divided into five groups (eight rats each). Group I received saline (0.

Exercise and Stevia Rebaudiana (R) Extracts Attenuate Diabetic Cardiomyopathy in Type 2 Diabetic Rats: Possible Underlying Mechanisms.

Background And Aims: In the current work, we studied the effects of exercise and stevia rebaudiana (R) extracts on diabetic cardiomyopathy (DCM) in type 2 diabetic rats and their possible underlying mechanisms.

Methods: Thirty-two male Sprague Dawley rats were randomly allocated into 4 equal groups; a) normal control group, b) DM group, type 2 diabetic rats received 2 ml oral saline daily for 4 weeks, c) DM+ Exercise, type 2 diabetic rats were treated with exercise for 4 weeks and d) DM+ stevia R extracts: type 2 diabetic rats received methanolic stevia R extracts. By the end of the experiment, serum blood glucose, HOMA-IR, insulin and cardiac enzymes (LDH, CK-MB), cardiac histopathology, oxidative stress markers (MDA, GSH and CAT), myocardial fibrosis by Masson trichrome, the expression of p53, caspase-3, α-SMA and tyrosine hydroxylase (TH) by immunostaining in myocardial tissues were measured.

Vanadyl sulphate ameliorates biomarkers of endothelial injury and coagulation and thrombosis in a rat model of hyperglycaemia.

Background: We sought to determine whether the insulin mimicking agent, vanadyl sulphate (Van) can inhibit biomarkers of endothelial injury and coagulation and thrombosis induced by a moderate level of hyperglycaemia.

Material And Methods: Hyperglycaemia was induced in rats by a single injection of streptozotocin (STZ, 50 mg/kg) two weeks after being fed on a high-fat diet (model group). The treatment group started Van (20 mg/kg/day) treatment one-week post STZ injection and continued on Van until being sacrificed at week 10.

Metformin suppresses aortic ultrastrucural damage and hypertension induced by diabetes: a potential role of advanced glycation end products.

Cardiovascular disease secondary to diabetes represents a significant challenge to the health community. The advanced glycation end products (AGEs) play an important role in diabetes-mediated vascular injury. We tested whether metformin can suppress aortic AGEs production and protect against aortic injuries (aortopathy) and hypertension in streptozotocin-induced type 2 diabetes mellitus (T2DM) animal model.

Insulin protects against type 1 diabetes mellitus-induced aortopathy associated with the inhibition of biomarkers of vascular injury in rats.

Background: We sought to investigate the protective effect of insulin against type 1 diabetes mellitus (T1DM)-induced aortic injury (aortopathy) associated with the inhibition of biomarkers of vascular injury.

Material And Methods: T1DM was induced in rats by streptozotocin (STZ) (65 mg/kg), and the protection group started insulin treatment 2 days post diabetic induction and continued until being sacrificed at week 8.

Results: Aortopathy was developed in the diabetic rats as demonstrated by profound alterations to the aorta ultrastructure, which was substantially protected by insulin.

Vitamin E ameliorates alterations to the articular cartilage of knee joints induced by monoiodoacetate and diabetes mellitus in rats.

We recently reported an animal model of osteoarthritis (OA) induced by a combination of the chondrocyte glycolysis inhibitor, monoiodoacetate (MIA) and the agent that induces diabetes mellitus, streptozotocin (STZ). Here we investigated the potential protective effect of the antioxidant and anti-inflammatory agent, vitamin E against MIA+STZ-induced OA. Therefore, rats were either injected once with MIA (2 mg/50 μL) + 65 mg/kg STZ before being sacrificed after 8 weeks (model group) or were treated immediately after MIA+STZ injections with vitamin E (600 mg/kg; thrice a week) before being sacrificed after 8 weeks (treatment group).

Natural Hypoxia is Not a Limiting Factor in Evaluating the Novel Arylidene Derivative MLT-401 Against an In Vitro Colorectal Cancer Model.

Background/aims: Cancer cells in vivo develop resistance to many anti-tumor drugs. One known factor to influence such drug resistance is hypoxia, which is an important component of the tumor microenvironment. Standard cancer lines mostly do not exhibit a cellular hypoxic microenvironment and there is a paucity of information on the efficacy of lead molecules in both cellular- and environment-induced hypoxic conditions.

Ghrelin prevents cardiac cell apoptosis during cardiac remodelling post experimentally induced myocardial infarction in rats via activation of Raf-MEK1/2-ERK1/2 signalling.

Context: Mechanisms by which ghrelin affords its cardioprotection in mammals remained unclear.

Objective: To examine if ghrelin confers cardio-protection during cardiac remodelling post-MI by modulating the RAF-1-MEK1/2-ERK1/2 signalling pathway.

Materials And Methods: Rats were divided into control, sham, sham + ghrelin, myocardial infarction (MI), and MI + ghrelin groups.

Swim exercise inhibits hemostatic abnormalities in a rat model of obesity and insulin resistance.

Background: We sought to determine whether swim exercise can inhibit high carbohydrate and fat diet (HCFD)-induced biomarkers of coagulation and thrombosis.

Material And Methods: Rats were either fed with HCFD (model group) or a standard laboratory chow (control group) for 15 weeks. Swim exercise-'treated' rats started swim exercise training from the 11 week until being sacrificed, on Week 15.

Swim exercise training ameliorates hepatocyte ultrastructural alterations in rats fed on a high fat and sugar diet.

Excessive consumption of carbohydrate and fat increases the risk of liver disease. We hypothesized that swim exercise can protect hepatocytes from ultra-structural damage induced by high cholesterol and fructose diets (HCFD). Rats were either fed with HCFD (model group) or a standard laboratory chow (control group) for 15 weeks before being sacrificed.

Modulatory Effect of Concomitant Administration of Insulin and Vanadium on Inflammatory Biomarkers in Type 2 Diabetic Rats: Role of Adiponectin.

The aim of this study is to investigate the effect of vanadium and/or insulin on the proinflammatory biomarkers in type 2 diabetes mellitus (T2DM) rat model. Sixty male Sprague Dawley rats were divided into six groups (n = 10). Control group, control vanadium group, T2DM group, insulin-treated diabetic group, vanadium-treated diabetic group, and concomitant insulin and vanadium-treated diabetic group.

MSCs ameliorates DPN induced cellular pathology via [Ca ] homeostasis and scavenging the pro-inflammatory cytokines.

The MSCs of various origins are known to ameliorate or modulate cell survival strategies. We investigated, whether UCB MSCs could improve the survival of the human neuronal cells and/or fibroblast assaulted with DPN sera. The results showed, the co-culture of UCB MSCs with human neuronal cells and/or fibroblasts could effectively scavenge the pro-inflammatory cytokines TNF-α, IL-1β, IFN-ɤ and IL - 12 and control the pro-apoptotic expression of p53/Bax.

Modulation of the neurological and vascular complications by grape seed extract in a rat model of spinal cord ischemia-reperfusion injury by downregulation of both osteopontin and cyclooxygenase-2.

In this study, we investigated the effects of grape seed extract (GSE) on the expression of osteopontin (OPN) and cyclooxygenase-2 (COX-2) in a rat model of spinal cord ischemia-reperfusion injury (SC-IRI). Fifty male rats were divided into 5 groups: control (CON); control + GSE (CON + GSE) (received GSE for 28 days); sham operated (Sham); IRI; and IRI + GSE. SC-IRI was induced by clamping the aorta just above the bifurcation for 45 min, and then the clamp was released for 48 h for reperfusion.

Insulin and vanadium protect against osteoarthritis development secondary to diabetes mellitus in rats.

Objective: Diabetic complications such as cardiovascular disease and osteoarthritis (OA) are among the common public health problems. The effect of insulin on OA secondary to diabetes has not been investigated before in animal models. Therefore, we sought to determine whether insulin and the insulin-mimicking agent, vanadium can protect from developing OA in diabetic rats.

Resveratrol reverses cadmium chloride-induced testicular damage and subfertility by downregulating p53 and Bax and upregulating gonadotropins and Bcl-2 gene expression.

This study was performed to investigate the protective and therapeutic effects of resveratrol (RES) against CdCl2-induced toxicity in rat testes. Seven experimental groups of adult male rats were formulated as follows: A) controls+NS, B) control+vehicle (saline solution of hydroxypropyl cyclodextrin), C) RES treated, D) CdCl2+NS, E) CdCl2+vehicle, F) RES followed by CdCl2 and M) CdCl2 followed by RES. At the end of the protocol, serum levels of FSH, LH and testosterone were measured in all groups, and testicular levels of TBARS and superoxide dismutase (SOD) activity were measured.

Acute exposure to Catha edulis depresses contractility and induces myocardial infarction in spontaneously contracting, isolated rabbit's heart.

Khat chewing is a recreational habit known to pose major socio-economic and medical problems in countries of Southern Arabia and the Horn of Africa. Among other adverse health effects, khat chewing has been associated with an increased risk of myocardial infarction (MI) in heavy consumers. This study was carried out to examine the direct effects of Catha edulis extract on contractility of spontaneously contracting, isolated rabbit heart and to investigate its mechanism of action.

In vivo acute effects of orally administered hydro-ethanol extract of Catha edulis on blood glucose levels in normal, glucose-fed hyperglycemic, and alloxan-induced diabetic rats.

Objective: To investigate the blood glucose lowering effect of khat (Catha edulis) extract in normal, glucose-loaded, and alloxan diabetic rats.

Methods: Three experimental protocols were used in this study. In each of the first 2 protocols, 3 groups of rats (6 rats per group) were used as control group (NS), Catha edulis (CE) treated, and glibenclamide treated groups.

Cardiac adaptive responses after hypoxia in an experimental model.

The role of vascular endothelial growth factor (VEGF) and erythropoietin (EPO) in mediating hypoxic preconditioning under the acute intermittent hypoxic condition (AIH) was investigated in this study. Male Wistar rats were randomly assigned and kept in normoxic conditions, (Nx) or in AIH conditions and subjected to brief cycles hypoxia/reoxygenation. Hearts were isolated, perfused, and subjected to in vitro global ischemia followed by reperfusion.

Effect of hyperoxia on the ultrastructural pathology of alveolar epithelium in relation to glutathione peroxidase, lactate dehydrogenase activities, and free radical production in rats, Rattus norvigicus.

Hyperoxia (HP) exposure inducts reactive oxygen species (ROS) in the lungs that may result in lung injury, including alveolar epithelial and endothelial cells. Lactate dehydrogenase (LDH) activity relates to glycolysis, whereas glutathione peroxidase (Gpx) activity relies on the pentose phosphate pathway (PPP). The purpose of this study was to examine early ROS-induced alveolar pathological changes in relation to the activity of glutathione peroxidase (GPx) and lactate dehydrogenase (LDH) activity.

Oxidative stress as a common mediator for apoptosis induced-cardiac damage in diabetic rats.

Aim: To investigate the possible role of oxidative stress as a common mediator of apoptosis and cardiac damage in diabetes.

Materials And Methods: This experimental work was conducted on 5 groups of Wistar rats. Group I was the control group.

Adequate stimuli of the carotid body: more than an oxygen sensor?

The past 10-20 years has seen a significant increase in the number of studies aimed at elucidating the mechanism of action of the carotid body and this has led to an increased knowledge of how this sensory organ transduces hypoxaemia into afferent chemodischarge. Whilst hypoxia is often considered as the most significant, peripheral chemostimulus, the carotid body is able to transduce many other physico-chemical stimuli, including not only arterial P(CO2) and pH but also blood potassium concentration, temperature and osmolarity as well as, potentially, blood glucose levels and all with appropriate physiological sensitivity. Although it is difficult to be definitive, these other stimuli appear to be sensed independently of the hypoxia transduction process, albeit converging at the point of type I cell membrane depolarisation or Ca(2+) -dependent neurosecretion.