Explore the vast range of titles available.

Exposure to the herbicide atrazine (ATZ) has deleterious effects on male fertility. This fact underscores the need for measures to protect against the detrimental impact of atrazine exposure on male fertility. The study assessed the protective effects of plantain-based diet (PBD) on rat testes exposed to ATZ by exploring oxid-inflammatory homeostasis. The study evaluated the preventive and therapeutic effects of PBD in a two-phased experiment. Male rats were randomized into seven groups for therapeutic model (Control, ATZ only, ATZ recovery, ATZ + 50% PBD, ATZ + 25% PBD, ATZ + 12.5% PBD and ATZ + quercetin-QUE) while the preventive model had ten groups (Control, ATZ, 50% PBD + ATZ, 25% PBD + ATZ, 12.5% PBD + ATZ and QUE + ATZ). The oxidative stress parameters (DNA fragmentation and MDA level), purinergic activity (ATPase), acetylcholine esterase, and inflammatory markers (NO level, MPO activity, and TNF-α) were increased while the Nrf2 levels were decreased by the ATZ treatment. However, the PBD was able to restore the oxido-inflammatory parameters in the rat testes. The chemical fingerprint of the diet revealed that the diets contained 16 bioactive compounds with quercetin being the most prominent compound. Overall, treatment with PBD was able to protect and prevent the toxicity caused by ATZ by modulating the redox and inflammatory status as well as purinergic activity in the rat testes.

Cadmium is a highly neurotoxic heavy metal that disrupts membranes and causes oxidative stress in the brain. The study aimed to investigate the neuroprotective effect of gallic acid on oxidative damage in the brains of Wistar rats exposed to cadmium chloride (CdCl 2 ). Male Wistar rats were divided into four groups of five rats each. Group 1 was administered distilled water only throughout the study. Throughout the study, Group 2 received CdCl 2 alone (5 mg/kg b.w./day), Group 3 received gallic acid (20 mg/kg b.w./day), and Group 4 received CdCl 2  + gallic acid (20 mg/kg). Treatments were oral with distilled water as a vehicle. The study lasted 21 days. In the brain, the activities of cholinesterase and antioxidant enzymes were evaluated, as well as the levels of reduced glutathione, malondialdehyde, neurotransmitters, Na+/K+ ATPase, myeloperoxidase activity, nitric oxide, and interleukin-6. CdCl 2 -induced brain impairments in experimental animals and gallic acid prevents the following CdCl 2 -induced activities: inhibition of acetylcholinesterase (AChE) and butyrylcholinesterase (BChE), elevated neurotransmitters (serotonin and dopamine), decreased antioxidant enzymes (superoxide dismutase, catalase), decreased glutathione, Na+/K+ ATPases, and increased MDA and neuroinflammatory markers (myeloperoxidase (MPO), nitric oxide, and interleukin-6 in the brain of experimental rats exposed to CdCl 2 ( p  < 0.05). Taken together, the neuroprotective effects of gallic acid on CdCl 2 -induced toxicity in the brains of rats suggest its potent antioxidant and neurotherapeutic properties.

Reactive species, such as those of oxygen, nitrogen, and sulfur, are considered part of normal cellular metabolism and play significant roles that can impact several signaling processes in ways that lead to either cellular sustenance, protection, or damage. Cellular redox processes involve a balance in the production of reactive species (RS) and their removal because redox imbalance may facilitate oxidative damage. Physiologically, redox homeostasis is essential for the maintenance of many cellular processes. RS may serve as signaling molecules or cause oxidative cellular damage depending on the delicate equilibrium between RS production and their efficient removal through the use of enzymatic or nonenzymatic cellular mechanisms. Moreover, accumulating evidence suggests that redox imbalance plays a significant role in the progression of several neurodegenerative diseases. For example, studies have shown that redox imbalance in the brain mediates neurodegeneration and alters normal cytoprotective responses to stress. Therefore, this review describes redox homeostasis in neurodegenerative diseases with a focus on Alzheimer’s and Parkinson’s disease. A clearer understanding of the redox-regulated processes in neurodegenerative disorders may afford opportunities for newer therapeutic strategies.

Alzheimer’s disease (AD) is an age-associated neurodegenerative condition marked by amyloid plaques, synaptic dysfunction, and neuronal loss. Besides conventional medical care, herbal therapies, both raw and refined, have attracted researchers for their potential therapeutic effects. As a proof-of-concept, our study combined HPLC-DAD analysis of bioactive constituents, network pharmacology, molecular dynamics (MD), molecular docking, post-MD analysis, and experimental verification to investigate the mechanisms of crude drug formulations as a therapeutic strategy for AD. We identified nine bioactive compounds targeting 188 proteins and 1171 AD-associated genes. Using a Venn diagram, we found 47 overlapping targets, forming “herb-compound-target (HCT)” interaction networks and a protein‒protein interaction (PPI) network. Simulations analyzed binding interactions among the three core targets and their compounds. MD assessed the stability of the best-ranked poses and beneficial compounds for each protein. Among the top 22 hub genes, AChE, BChE, and MAO, ranked 10, 14, and 34, respectively, were selected for further analysis. Two tetraherbal formulations, Form A and Form B, showed notable activity against AChE. Form A exhibited significant (p < 0.0001) inhibitory activity (IC50 = 114.842 ± 2.084 µg/mL) compared to Form B (IC50 = 142.829 ± 4.258 µg/mL), though weaker than galantamine (IC50 = 27.950 ± 0.122 µg/mL). Form B had significant inhibitory effects on BChE (IC50 = 655.860 ± 32.812 µg/mL) compared to Form A (IC50 = 679.718 ± 20.656 µg/mL), but lower than galantamine (IC50 = 23.126 ± 0.683 µg/mL). Both forms protected against Fe2+-mediated brain injury by inhibiting MAO. Docking identified quercetin (−10.2 kcal/mol) and myricetin (−10.1 kcal/mol) for AChE; rutin (−10.6 kcal/mol) and quercetin (−9.7 kcal/mol) for BChE; and kaempferol (−9.1 kcal/mol) and quercetin (−8.9 kcal/mol) for MAO. These compounds were thermodynamically stable based on MD analysis. Collectively, the results offer a scientific rationale for the use of these specifically selected medicinal herbs as AD medications.

Neurodegenerative diseases (NDs) like Alzheimer’s disease, multiple sclerosis, amyotrophic lateral sclerosis, Parkinson’s disease, and Huntington’s disease predominantly pose a significant socioeconomic burden. Characterized by progressive neural dysfunction coupled with motor or intellectual impairment, the pathogenesis of ND may result from contributions of certain environmental and molecular factors. One such condition is hypoxia, characterized by reduced organ/tissue exposure to oxygen. Reduced oxygen supply often occurs during the pathogenesis of ND and the aging process. Despite the well-established relationship between these two conditions (i.e., hypoxia and ND), the underlying molecular events or mechanisms connecting hypoxia to ND remain ill-defined. However, the relatedness may stem from the protective or deleterious effects of the transcription factor, hypoxia-inducible factor 1-alpha (HIF-1α). The upregulation of HIF-1α occurs in the pathogenesis of most NDs. The dual function of HIF-1α in acting as a “killer factor” or a “protective factor” depends on the prevailing local cellular condition. The kynurenine pathway is a metabolic pathway involved in the oxidative breakdown of tryptophan. It is essential in neurotransmission and immune function and, like hypoxia, associated with ND. Thus, a good understanding of factors, including hypoxia (i.e., the biochemical implication of HIF-1α) and kynurenine pathway activation in NDs, focusing on Alzheimer’s disease could prove beneficial to new therapeutic approaches for this disease, thus the aim of this review.

The study investigated the effects of Zingiber officinale root and Vernonia amygdalina leaf on the brain redox status of Wistar rats. Twenty-four (24) rats weighing 160 ± 20 g were randomly assigned into four (4) groups, each with six (6) rats. Animals in Group 1 (control) were orally administered distilled water (1 mL), while the test groups were orally administered 5 mg/mL of either Z. officinale, V. amygdalina infusion, or a combination of both, respectively, for 7 days. The rats were sacrificed at the end of treatments and blood and tissue were harvested and prepared for biochemical assays. Results showed that administration of V. amygdalina and Z. officinale, as well as their coadministration, reduced the levels of malondialdehyde (MDA), nitric oxide (NO), acetylcholinesterase (AChE), and myeloperoxidase (MPO) in rat brain tissue compared with the control group. Conversely, coadministration of V. amygdalina and Z. officinale increased the levels of reduced glutathione (GSH) in rat brain tissue compared with the control group. However, the administration of the infusions singly, as well as the combination of both infusions, did not have any effect on the rat brain levels of glutathione peroxidase (GPx) and catalase (CAT) antioxidant enzymes compared to the control. Taken together, the findings indicate that the V. amygdalina and Z. officinale tea infusions have favorable antioxidant properties in the rat brain. The findings are confirmatory and contribute to deepening our understanding of the health-promoting effects of V. amygdalina and Z. officinale tea infusions.

Silver nanoparticles are increasingly being used in a wide variety of ways that may lead to frequency of exposure for humans and the environment. Thus, it is necessary to understand the biological effect(s) of these nanoparticles. Previously, we showed that AgNPs activated the kynurenine pathway in rat brain independently of oxidative stress in rats. This present study is aimed at evaluating the effect of AgNPs on some selected cytokines, redox parameters, and on the kynurenine level in rats. Male Wistar rats (130-150 g) were divided into 4 groups. Rats were grouped into control, AgNPs only (50 mg/kg bw), coadministration of AgNPs (50 mg/kg bw), and dexamethasone (100 mg/kg bw) and dexamethasone only (100 mg/kg bw). Results indicated that AgNPs did not significantly elevate MDA levels in rat plasma and brain relative to the control group. AgNPs caused a significant alteration in the level of rat brain and plasma total protein concentration. Meanwhile, AgNPs led to an elevation in the level of reduced glutathione (GSH) in rat plasma but decreased plasma kynurenine level significantly. Furthermore, IFN-γ level was reduced following AgNPs administration, IL-1β decreased across the treatment groups, while NF-κB was reduced in the dexamethasone only and AgNPs+dexamethasone groups when compared with the control. AgNPs led to increased IL-4 levels, while IL-10 levels decreased across the treatment groups. Taken together, our data showed a differential immunomodulatory potential of AgNPs in rats.

Research into the impacts of oxidative stress (OS), and hormonal balance on reproductive potential has increased over the last 40 years possibly due to rising male infertility. Decreased antioxidant levels and increased OS in tissues result from hormonal imbalance, which in turn leads to male infertility. Increased reactive oxygen species (ROS) generation in seminal plasma has been linked to many lifestyle factors such as alcohol and tobacco use, toxicant exposure, obesity, varicocele, stress, and aging. This article provides an overview of the crosslink between OS and gonadal hormone disruption, as well as a potential mode of action in male infertility. Disrupting the equilibrium between ROS generation and the antioxidant defense mechanism in the male reproductive system may affect key hormonal regulators of male reproductive activities. Unchecked ROS production may cause direct injury on reproductive tissues or could disrupt normal regulatory mechanisms of the hypothalamic-pituitary–gonadal (HPG) axis and its interaction with other endocrine axes, both of which have negative effects on male reproductive health and can lead to male infertility.

Plants have been used in various regions of the world to treat various medical conditions including male infertility. The review aims to evaluate the pharmacological effects of watermelon consumption in improving male fertility and sexual function. Watermelon is a popular fruit consumed around the world for its diverse nutritional and health-promoting qualities. This study showed the mechanism via which watermelon enhances male fertility as it was reported for improving semen quality, reversing erectile dysfunction, enhancing testicular redox status, as well as improving gonadotropin secretion. These activities have been linked to their constituents as it contains vitamins and phytochemicals such as phenols and certain flavonoids that contribute to their antioxidant properties. Watermelon has also been noted to possess antimicrobial, anti-helminthic, antioxidant, antidiabetic, anti-inflammatory, and antihypertensive properties that may contribute to its therapeutic use.

This study assessed the effect of heat exposure on gonadal-related hormones in male and female Wistar rats. Twenty rats (140 - 160) were divided into 2 groups (male and female rats) and further sub-grouped into control and heat-exposed rats. Rats were exposed to heat for 4 hours daily for 21 days after which the rats were necropsied, and blood collected from the jugular veins. Heat exposure caused appreciable decreases in the levels of luteinizing hormones and follicle-stimulating hormones in both the male and female rats., Also, heat exposure caused a decline in the level of testosterone in male rats and decreased progesterone and oestrogen in their female counterparts. Furthermore, heat exposure caused oxidative stress by elevating the levels of malondialdehyde and nitric oxide, but lowering the antioxidants such as catalase, superoxide dismutase and thiols in rats. This study thus showed that heat exposure significantly disrupts hormonal balance and induces oxidative stress in both male and female Wistar rats. Findings have implications for climate change impact on health.