Co Q10 improves vascular reactivity in male diabetic rats by enhancing insulin sensitivity and antioxidant effect.

Oxidative stress is the main player in the development of diabetic vascular complications. Co-Q10 is a natural antioxidant present in the body and in many foods. This study was designed to evaluate the effect of Co-Q10 administration to improve vascular complications and increase insulin sensitivity in diabetic rats. Fifty male rats were divided into five groups: control, diabetic untreated, diabetic insulin-treated, diabetic Co-Q10-treated, and diabetic combined-treated groups. After 8 weeks, blood pressure and vascular reactivity to NE and ACh, fasting glucose, insulin, C-peptide, MDA, TAC, HbA1c, and the HOMA-IR were measured. Diabetes increased fasting glucose, HbA1c, HOMA-IR, MDA, blood pressure, and decreased TAC and vascular reactivity. Ttreatment with insulin or Co-Q10 improved glycemic parameters and increasing antioxidant levels compared to diabetic group. Combined Co-Q10 with insulin was found to increase insulin sensitivity and decrease its resistance, which helps to decrease insulin doses in diabetic patients and reduce its side effects.

Effect of L-carnitine and atorvastatin on a rat model of ischemia-reperfusion injury of spinal cord.

Pro-inflammatory cytokines and reactive oxygen species (ROS) are produced in acute spinal cord injury, leading to myelin breakdown, inflammation, mitochondrial dysfunction, and apoptosis of neurons and glial cells. The aim of the present study was to investigate possible protective effects of L-carnitine (carn) or atorvastatin (ator) on spinal cord ischemia-reperfusion injury (IRI). Rats were randomized into nine equal groups (n = 8): control and control taking carn (100 mg/kg BW), ator (2.5 mg/kg BW) or both, as well as sham-operation, IRI and IRI taking same doses of carn, ator or both. Neurological assessments were done 48 hours after IRI, and serum nitrite/nitrate was measured. Finally, lumbar segments of spinal cord were excised, and part was homogenized and prepared for measuring tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß), malondialdehyde (MDA), advanced oxidation protein products (AOPP), reduced glutathione (GSH), glutathione peroxidase (GPx), superoxide dismutase (SOD) and catalase. The other part was sectioned for evaluation of histopathological changes and for immunostaining by glial fibrillary acidic protein (GFAP), Bax and Bcl-2. The IRI increased ROS (nitrite/nitrate, MDA, AOPP) and pro-inflammatory cytokines (TNF-α, IL-1ß), and decreased antioxidants (GSH, GPx, SOD, catalase) with impaired sensory and motor functions. Astrogliosis was detected by GFAP, and increased apoptosis was demonstrated by increasing Bax and decreasing Bcl-2. Treatment with carn or ator alone decreased TNF-α, IL-1ß, nitrite/nitrate, MDA and AOPP, and increased GSH, GPx, SOD, and catalase with improvement of neurological functions and histological studies. Combination of carn and ator improved most of measured IRI-affected parameters better than isolated carn or ator administration.

Intermittent Fasting Ameliorated High-Fat Diet-Induced Memory Impairment in Rats via Reducing Oxidative Stress and Glial Fibrillary Acidic Protein Expression in Brain.

Intermittent fasting (IF) plays an important role in the protection against metabolic syndrome-induced memory defects. This study aimed to assess the protective effects of both prophylactic and curative IF against high-fat diet (HFD)-induced memory defects in rats. The control group received a normal diet; the second group received a HFD; the third group was fed a HFD for 12 weeks and subjected to IF during the last four weeks (curative IF); the fourth group was fed a HFD and subjected to IF simultaneously (prophylactic IF). A high-fat diet significantly increased body weight, serum lipids levels, malondialdehyde (MDA) concentration, glial fibrillary acidic protein (GFAP) and H score in brain tissue and altered memory performance. In addition, it significantly decreased reduced glutathione (GSH) concentration in brain tissue and viability and thickness of pyramidal and hippocampus granular cell layers. However, both types of IF significantly decreased body weight, serum lipids, GFAP protein expression and H score and MDA concentration in brain tissue, and improved memory performance, while it significantly increased GSH concentration in brain tissue, viability, and thickness of pyramidal and granular cell layers of the hippocampus. This study indicated that IF ameliorated HFD-induced memory disturbance and brain tissue damage and the prophylactic IF was more potent than curative IF.

Neuroprotective Potential of Allium sativum against Monosodium Glutamate-Induced Excitotoxicity: Impact on Short-Term Memory, Gliosis, and Oxidative Stress.

This study evaluated the neuroprotective potential of Allium sativum against monosodium glutamate (MSG)-induced neurotoxicity with respect to its impact on short-term memory in rats. Forty male Wistar albino rats were assigned into four groups. The control group received distilled water. The second group was administered Allium sativum powder (200 mg/kg of body weight) orally for 7 successive days, then was left without treatment until the 30th day. The third group was injected intraperitoneally with MSG (4 g/kg of body weight) for 7 successive days, then left without treatment until the 30th day. The fourth group was injected with MSG in the same manner as the third group and was treated with Allium sativum powder in the same manner as the second group, simultaneously. Phytochemical analysis of Allium sativum powder identified the presence of diallyl disulphide, carvone, diallyl trisulfide, and allyl tetrasulfide. MSG-induced excitotoxicity and cognitive deficit were represented by decreased distance moved and taking a long time to start moving from the center in the open field, as well as lack of curiosity in investigating the novel object and novel arm. Moreover, MSG altered hippocampus structure and increased MDA concentration and protein expression of glial fibrillary acidic protein (GFAP), calretinin, and caspase-3, whereas it decreased superoxide dismutase (SOD) activity and protein expression of Ki-67 in brain tissue. However, Allium sativum powder prevented MSG-induced neurotoxicity and improved short-term memory through enhancing antioxidant activity and reducing lipid peroxidation. In addition, it decreased protein expression of GFAP, calretinin, and caspase-3 and increased protein expression of Ki-67 in brain tissues and retained brain tissue architecture. This study indicated that Allium sativum powder ameliorated MSG-induced neurotoxicity through preventing oxidative stress-induced gliosis and apoptosis of brain tissue in rats.

Monosodium glutamate induces cardiac toxicity via oxidative stress, fibrosis, and P53 proapoptotic protein expression in rats.

Monosodium glutamate (MSG) is widely used as food additive and flavor enhancer; however, consumption of high dose of MSG provokes oxidative stress in many organs and its safety and side effects on the body are still controversial. Therefore, it is crucial to investigate the long-lasting effects of MSG on cardiac muscle functions and structure. Forty male Wister albino rats were assigned into 3 groups. Control group was injected intraperitoneally with physiological saline for 7 days. Second group was injected intraperitoneally with MSG at a dose of 4 mg/g b.w/day for 7 consecutive days and then kept without any treatment till 45th day of the experiment. Third group was injected intraperitoneally with MSG at a dose of 6 mg/g b.w/day for 7 consecutive days and then kept without any treatment till 45th day of the experiment. Monosodium glutamate significantly reduced body weight, force of cardiac muscle contractility, serum level of high-density lipoprotein, and superoxide dismutase activity in cardiac muscle, while it significantly elevated heart rate, serum levels of total cholesterol, low-density lipoprotein, triacylglycerides, atherogenic index and troponin T, activities of serum lactate dehydrogenase and creatine kinase-MB, malondialdehyde concentration, and P53 protein expression in cardiac muscle. In addition, it induced myocardial degeneration, cellular infiltration, deposition of collagen in cardiac muscle, and periodic acid-Schiff staining reaction. This study indicated that MSG exerted long-lasting functional and structural alterations in the heart of male albino rats through induction of oxidative stress, atherogenesis, and apoptosis.