Obesity is a global epidemic disease that is closely associated with various health problems as Diabetes mellitus, cardiovascular, and metabolic disorders. Lycopene (LYC), a red-colored carotenoid, has demonstrated various promising therapeutic effects. Hence, the potential of LYC was studied against high fat diet (HFD)-induced obesity and metabolic disturbances in rats. Animals fed on HFD and orally supplemented with LYC (25 and 50 mg/kg) or simvastatin (10 mg/kg) every day for 3 months. The results revealed that long-term consumption of HFD significantly increased weight gain, liver weight, cholesterol, triglycerides (TG), apolipoprotein-B (Apo-B), low-density lipoprotein-cholesterol (LDL-c) levels, as well as decreasing the high-density lipoprotein-cholesterol (HDL-c) levels. Moreover, high blood glucose and insulin levels accompanied by low peroxisome proliferator activated receptor gamma (PPAR-γ) were recorded in HFD group. Further, HFD rats displayed lower levels of antioxidant biomarkers (SOD, CAT, GPx, GR and GSH), in addition to higher levels of MDA, NO and inflammatory mediators (IL-1β, TNF-α, and MPO). Marked increases were observed in atherogenic index, lactate dehydrogenase and creatine kinase together with fibrosis markers (TGF-β1 and α-SMA) in rats fed on HFD. Comparing to model group, LYC was able to effectively reverse HFD-mediated alterations at dose dependent manner. Altogether, dietary supplementation of LYC successfully reversed HFD-induced alterations through its antioxidant, anti-inflammatory, and anti-fibrotic properties. Hence, LYC displayed a therapeutic potential to manage obesity and its associated pathologies.

It is common for food to be made more palatable through the use of the flavour enhancer monosodium glutamate, also known as vetsin powder. The purpose of the study described in this paper was to explore how vetsin‐induced hepatic toxicity, DNA fragmentation, damage, and oxidative stress modifications could be mitigated with moringa leaf extract (MLE). To that end, 40 male rats were separated into four groups: normal control, positive control or MLE, vetsin, and vetsin combined with MLE. Results indicated that, compared to the control group, the levels of serum alanine aminotransferase (ALT), aminotransferase (AST), alkaline phosphatase (ALP), gamma‐glutamyl transferase (GGT), liver malondialdehyde (MDA), DNA damage, injury, PCNA, and P53 expressions were significantly enhanced by the administration of vetsin (P < 0.05). However, the vetsin group had significantly reduced levels of albumin, globulin, total protein, liver glutathione (GSH), superoxide dismutase enzyme (SOD), catalase, and glutathione S‐transferase (GST) enzyme activities (P < 0.05) by comparison to control. Meanwhile, modifications in liver functions, oxidative stress, DNA damage, liver injury, and PCNA expression were alleviated when vetsin was administered alongside MLE. The authors conclude that vetsin may have many side effects and that MLE can ameliorate biochemical changes, oxidative stress, hepatic injury, PCNA, and P53 alterations induced by vetsin administration.

A collection of metabolic disorders and neurodegenerative diseases linked to oxidative stress and neuroinflammation frequently affect postmenopausal women or estrogen deprivation. Recent research has focused on alternative therapies that can enhance these women’s quality of life. This study set out to investigate the effects of physical exercise (EX) and intermittent fasting (IF) on oxidants/antioxidants, inflammatory cytokines, neurotransmitters, and brain-derived neurotrophic factor (BDNF) in the cortex of rats. Additionally, it sought to assess the response to oxidative stress and neuroinflammation in the brains of rats following ovariectomy (OVX) and the potential mechanisms of these interventions. Fifty female rats were divided into one of the following groups 30 days after bilateral OVX: Control, OVX, OVX + EX, OVX + IF, and OVX + EX + IF groups. The rats in the Control and OVX groups continued their normal activities and had unrestricted access to food and water, but the rats in the OVX + EX and OVX + EX + IF groups had a 4-week treadmill training program, and the rats in the OXV + IF and OVX + EX + IF groups fasted for 13 h each day. The rats were killed, the cerebral cortex was taken, tissue homogenates were created, and various parameters were estimated using these homogenates. The results show that ovariectomized rats had decreased levels of neurotransmitters (DA, NE, and SE), acetylcholinesterase, brain GSH (glutathione), SOD (superoxide dismutase), catalase, GPx (glutathione peroxidase), and TAC (total antioxidant capacity), as well as elevated levels of proinflammatory cytokines and mediators (TNF-α, IL-1β, Cox-2). While ovariectomy-induced declines in neurotransmitters, enzymatic and nonenzymatic molecules, neuroinflammation, and oxidative brain damage were considerably mitigated and prevented by treadmill exercise and intermittent fasting, BDNF was significantly increased. These results suggest that ovariectomy can impair rat neuronal function and regular treadmill exercise and intermittent fasting seem to protect against ovariectomy-induced neuronal impairment through the inhibition of oxidative stress and neuroinflammation and increased BDNF levels in the brain cortex. However, combining regular exercise and intermittent fasting did not provide additional benefits compared to either treatment alone.

Introduction: Nanoparticles are at the forefront of rapidly developing nanotechnology and have gained much attention for their application as an effective drug delivery system and as a mediated therapeutic agent for cancer. However, the cytotoxicity of nanoparticles is still relatively unknown and, therefore, additional study is required in order to elucidate the potential toxicity of these nanoparticles on cells. Materials and Methods: Thus, the following work aimed to investigate the capability of Beta vulgaris (beetroot) water extract (BWE; 200 mg/kg) to protect hepatic tissue following silver nanoparticles (AgNPs; 80 mg/kg; > 100 nm) intoxication in male rats. Results: AgNPs-intoxication elevated the liver function markers – including serum transaminases and alkaline phosphatase activities – and decreased serum levels of albumin and total proteins, in addition to disturbing the oxidation homeostasis. This is evidenced by the increased lipid peroxidation, the depleted glutathione, and the suppressed activity of superoxide dismutase and catalase. In addition, an apoptotic reaction was observed following AgNPs treatment, as indicated by the up-regulation of p53 and down-regulating Bcl-2 expressions, examined by the immunohistochemistry method. Furthermore, AgNPs exhibited a marked elevation in liver DNA damage that was indicated by an increase in tail length, tail DNA% and tail movement. However, BWE eliminated the biochemical and histological alterations, reflecting its hepatoprotection effect in response to AgNPs. Discussion: Collectively, the present data suggest that BWE could be used following AgNPs as a potential therapeutic intervention to minimize AgNPs-induced liver toxicity.

The complicated disorder of hypercholesterolemia has several underlying factors, including genetic and lifestyle factors. Low LDL cholesterol and elevated serum total cholesterol are its defining features. A carotenoid with antioxidant quality is lycopene. Examining lycopene activity in an animal model of hypercholesterolemia induced using food was the aim of this investigation. Triglycerides, LDL cholesterol, HDL cholesterol, and plasma total cholesterol were all measured. Biomarkers of renal and cardiac function were also examined. Apoptotic indicators, pro-inflammatory markers, and oxidative stress were also assessed. Additionally, the mRNA expression of paraoxonase 1 (PON-1), peroxisome proliferator-activated receptor gamma (PPAR-γ), and PPAR-γ coactivator 1 alpha (PGC-1α) in cardiac and renal tissues was examined. Rats showed elevated serum lipid levels, renal and cardiac dysfunction, significant oxidative stress, and pro-inflammatory and apoptotic markers at the end of the study. Treatment with lycopene significantly corrected and restored these changes. Additionally, lycopene markedly increased the mRNA expression of PGC-1α and PON-1, and decreased PPAR-γ expression. It was determined that lycopene has the capacity to modulate the PPAR-γ and PON-1 signaling pathway in order to preserve the cellular energy metabolism of the heart and kidney, which in turn reduces tissue inflammatory response and apoptosis. According to these findings, lycopene may be utilized as a medication to treat hypercholesterolemia. However, further studies should be conducted first to determine the appropriate dose and any adverse effects that may appear after lycopene usage in humans.

The frequency of overweight and obesity is rising globally. These disorders are prevalent health problems. It has a substantial correlation with a number of health issues, including cardiovascular, metabolic, and diabetes mellitus disorders. Lycopene (Lyc) is an acyclic structural isomer of β-carotene and has powerful antioxidant properties with various promising therapeutic effects. In this study, rats fed a high-fat diet were examined to determine how lycopene affected metabolic syndrome and kidney damage. After being acclimated, rats were divided into 5 groups (n = 8/group) as follows: the first group served as the control and was fed on a normal pelleted diet (4.25% fat) until the end of the experiment. The second group (high-fat diet; HFD) was fed on a high-fat diet (45.5 kcal% fat) composed of 24% fat, 24% protein, and 41% carbohydrate. The third and fourth groups were fed on HFD and administered lycopene at 25 and 50 mg/kg bodyweight orally every day. The fifth group (standard drug group) received HFD and simvastatin (SVS; 10 mg/kg bodyweight orally daily) for 3 months. Tissue samples from the kidney were taken for determination of the biochemical parameters, lipid peroxidation (LPO), protein carbonyl (PC), reduced glutathione (GSH), total thiol group, antioxidant enzymes, namely, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione reductase (GR), in addition to renal mRNA expression of nuclear factor erythroid 2-related factor 2 (Nrf2), renal levels of inflammatory markers [tumor necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1β), and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB)], and apoptotic markers (BCL2 Associated X (Bax), B-cell lymphoma 2 (Bcl-2), and Bax/Bcl-2 ratio). When compared to the control group, the HFD group's food consumption, body weight, serum levels of glucose, uric acid, creatinine, LPO, PC, TNF-α, IL-1β, Bax, and the Bax/Bcl-2 ratio all increased significantly. In the kidney sample of HFD-fed rats, there was a downregulation of Nrf2 mRNA expression along with a significant reduction in the enzymatic activity of SOD, CAT, GR, and GPx. Lyc treatment was able to successfully reverse HFD-mediated changes as compared to the HFD group. Consuming lyc helps to prevent fat and renal damage in a positive way.