Free Radical Oxidative Stress Research Articles

Chitosan-based hydrogel dressings with antibacterial and antioxidant for wound healing

Bacterial infection and free radical oxidative stress at the wound site could easily cause cascade inflammation and hinder the healing process of the wound. In this study, chitosan-cysteine-gallic acid (CCG) hydrogel with antibacterial and antioxidant properties was synthesized by chitosan (CS), cysteine (Cys), and gallic acid (GA) for a preliminary evaluation of its therapeutic efficacy in a mouse model of full-layer skin defect. In vitro analysis showed that the CCG hydrogel had good antibacterial activity and blood compatibility. In vivo, the CCG hydrogel wound dressings accelerated wound healing, stimulate angiogenesis, increase collagen deposition and anti-inflammatory factor expression. The CCG hydrogel wound dressing is designed to promote the regeneration of damaged skin tissue and is expected to become a potential candidate for clinical treatment.

Verifying the cytotoxicity of a biodegradable zinc alloy with nanodiamond sensors

Metals are widely utilized as implant materials for bone fixtures as well as stents. Biodegradable versions of these implants are highly desirable since patients do not have to undergo a second surgery for the materials to be removed. Attractive options for such materials are zinc silver alloys since they also offer the benefit of being antibacterial. However, it is important to investigate the effect of the degradation products of such alloys on the surrounding cells, taking into account silver cytotoxicity. Here we investigated zinc alloyed with 1 % of silver (Zn1Ag) and how differently concentrated extracts (1 %–100 %) of this material impact human umbilical vein endothelial cells (HUVECs). More specifically, we focused on free radical generation and oxidative stress as well as the impact on cell viability. To determine free radical production we used diamond-based quantum sensing as well as conventional fluorescent assays. The viability was assessed by observing cell morphology and the metabolic activity via the MTT assay. We found that 1 % and 10 % extracts are well tolerated by the cells. However, at higher extract concentrations we observed severe impact on cell viability and oxidative stress. We were also able to show that quantum sensing was able to detect significant free radical generation even at the lowest tested concentrations.

Mitochondrial Dysfunction as the Major Basis of Brain Aging.

The changes in the properties of three biological events that occur with cerebral aging are discussed. These adverse changes already begin to develop early in mid-life and gradually become more pronounced with senescence. Essentially, they are reflections of the progressive decline in effectiveness of key processes, resulting in the deviation of essential biochemical trajectories to ineffective and ultimately harmful variants of these programs. The emphasis of this review is the major role played by the mitochondria in the transition of these three important processes toward more deleterious variants as brain aging proceeds. The immune system: the shift away from an efficient immune response to a more unfocused, continuing inflammatory condition. Such a state is both ineffective and harmful. Reactive oxygen species are important intracellular signaling systems. Additionally, microglial phagocytic activity utilizing short lived reactive oxygen species contribute to the removal of aberrant or dead cells and bacteria. These processes are transformed into an excessive, untargeted, and persistent generation of pro-oxidant free radicals (oxidative stress). The normal efficient neural transmission is modified to a state of undirected, chronic low-level excitatory activity. Each of these changes is characterized by the occurrence of continuous activity that is inefficient and diffused. The signal/noise ratio of several critical biological events is thus reduced as beneficial responses are gradually replaced by their impaired and deleterious variants.

Unveiling Innovative Approaches to Mitigate Metals/Metalloids Toxicity for Sustainable Agriculture.

Due to anthropogenic activities, environmental pollution of heavy metals/metalloids (HMs) has increased and received growing attention in recent decades. Plants growing in HM-contaminated soils have slower growth and development, resulting in lower agricultural yield. Exposure to HMs leads to the generation of free radicals (oxidative stress), which alters plant morpho-physiological and biochemical pathways at the cellular and tissue levels. Plants have evolved complex defense mechanisms to avoid or tolerate the toxic effects of HMs, including HMs absorption and accumulation in cell organelles, immobilization by forming complexes with organic chelates, extraction via numerous transporters, ion channels, signaling cascades, and transcription elements, among others. Nonetheless, these internal defensive mechanisms are insufficient to overcome HMs toxicity. Therefore, unveiling HMs adaptation and tolerance mechanisms is necessary for sustainable agriculture. Recent breakthroughs in cutting-edge approaches such as phytohormone and gasotransmitters application, nanotechnology, omics, and genetic engineering tools have identified molecular regulators linked to HMs tolerance, which may be applied to generate HMs-tolerant future plants. This review summarizes numerous systems that plants have adapted to resist HMs toxicity, such as physiological, biochemical, and molecular responses. Diverse adaptation strategies have also been comprehensively presented to advance plant resilience to HMs toxicity that could enable sustainable agricultural production.

Identification of a novel oligopeptide from defatted walnut meal hydrolysate as a potential neuroprotective agent.

Free radical damage and oxidative stress are thought to play a crucial role in the development of neurodegenerative diseases. Walnut peptides, especially walnut oligopeptides, have been shown to protect nerve cells from oxidative stress and inflammatory damage, as well as improve memory function. In this study, walnut peptides were obtained from walnut meal through enzymatic hydrolysis, ultrafiltration, and gel filtration chromatography. A novel oligopeptide called AQ was successfully isolated and its chemical structure was identified as AASCDQ using ESI-MS/MS. AQ demonstrated remarkable scavenging activity against O2- free radicals (81.00%), DPPH free radicals (79.40%), and ABTS free radicals (67.09%) at a concentration of 1 mg mL-1. Furthermore, AQ exhibited strong neuroprotective effects against hydrogen peroxide-induced damage in SH-SY5Y cells, reducing cell injury and apoptosis. AQ also effectively inhibited the secretion of pro-inflammatory factors NO (IC50 = 46.03 ± 0.32 μM) and suppressed the expression of IL-6 and TNF-α in RAW264.7 cells stimulated by LPS. In vivo experiments demonstrated that AQ promoted angiogenesis in the quail chick chorioallantoic membrane assay and reduced ROS accumulation in Caenorhabditis elegans, thereby extending its lifespan. The anti-inflammatory mechanism of AQ was further confirmed by western blotting. In summary, the novel oligopeptide AQ possesses potential neuroprotective effects, including antioxidant, anti-inflammatory, angiogenic, and anti-aging properties, making it a promising candidate for the development of functional foods and pharmaceutical products.

Pengaruh Minyak Ikan Dan Minyak Krill Terhadap Kadar Malondialdehid Pada Tikus Putih (Rattus novergicus) Hiperglikemik

Hyperglycemia is a condition due to glucose levels in the blood exceeding normal levels. Chronic hyperglycemia will result in increased production of free radicals resulting in oxidative stress. Malondialdehyde (MDA) is a free radical biomarker and oxidative stress in the body. Fish oil and krill oil are anti-inflammatory and antioxidant properties. This study aims to determine the effect of fish oil and krill oil on the levels of Malondialdehyde in Wistar White Rats (Rattus novergicus) hyperglycemic. This study uses a true experimental research type pre and post control. The samples in this study were 24 white wistar rats (Rattus norvegicus) which were divided into 4 groups each consisting of 6 mice, namely the negative control group was given a placebo, the positive control group was given glibenclamide, the fish oil group was given fish oil and the oil group krill was given intervention krill oil for 14 days. The mean malondialdehyde (MDA) levels in each group were negative control group 2.47 μmol / l, positive control group 2.13 μmol / l, fish oil group 1.29 μmol / l and irill oil group 0.77 μmol / l. Based on the results of the One way Anova analysis, a significant value of p less than 0.05 was obtained. Fish oil and krill oil have an effect on reducing levels of malondialdehyde. However, krill oil is more effective in reducing malondialdehyde levels than fish oil.

Molecular mechanisms of NMDA excitotoxicity in the retina

NMDA excitotoxicity, as a part of glutamate excitotoxicity, has been proposed to contribute significantly to many retinal diseases. Therefore, understanding mechanisms of NMDA excitotoxicity will provide further insight into the mechanisms of many retinal diseases. To study mechanisms of NMDA excitotoxicity in vivo, we used an animal model in which NMDA (20 mM, 2 µL) was injected into the vitreous of mice. We also used high-throughput expression profiling, various animals with reduced expression of target genes, and animals treated with the oral iron chelator deferiprone. We found that the expression of many genes involved in inflammation, programmed cell death, free radical production, oxidative stress, and iron and calcium signaling was significantly increased 24 h after NMDA treatment. Meanwhile, decreased activity of the pro-inflammatory TNF signaling cascade and decreased levels of ferrous iron (Fe2+, required for free radical production) led to significant neuroprotection in NMDA-treated retinas. Since increased TNF signaling activity and high Fe2+ levels trigger regulated necrosis, which, in turn, lead to inflammation, we proposed an important role in NMDA excitotoxicity of a positive feedback loop in which regulated necrosis promotes inflammation, which subsequently triggers regulated necrosis.

Abstract P318: INDOLE-3 ACETIC ACID: A NOVEL DUAL-ACTION INHIBITOR OF THE ENDOTHELIN SYSTEM FOR TREATING HYPERTENSION

Elevated levels of endothelin-1 (ET-1) stimulate potent vasoconstriction, free radical production, oxidative stress, and vascular inflammation, which are often present in salt-sensitive hypertension, pulmonary hypertension, drug-resistant hypertension, and hypertension among African Americans. There is currently no known drug that simultaneously targets both ET-1 receptors (ETRs) and the ET-1 synthesizing enzyme ECE-1, even though dual targeting of the ET system could lead to a new generation of drug molecules with improved therapeutic outcome. Using an integrated in vitro, in vivo and in silico approaches, here we report the discovery of indole-3 acetic acid (IAA) as an inhibitor of both ET-1 receptors and ECE-1. IAA is produced in the human body via tryptophan metabolism by gut microbiota. Our data demonstrates that IAA concentration-dependently inhibits ET-1-evoked vasoconstriction in rat resistance mesenteric arteries and ET-1-stimulated reactive oxygen species (ROS) production in smooth muscle cells (SMCs). Furthermore, IAA suppresses ET-1-induced endothelial cell (EC) activation, adhesion molecule overexpression, and leukocyte adhesion. IAA inhibits ET-1-stimulated, ET A R- and ET B R-mediated increases in [Ca 2+ ] i . Intriguingly, IAA produces a concentration-dependent inhibition of purified human ECE-1. Treatment of Dahl salt-sensitive (DSS) hypertensive rats, a model of augmented ET-1 signaling, with an oral extended-release formulation of IAA significantly inhibits blood pressure elevation in high-salt diet-fed (HSD) DSS rats. IAA-treated DSS arteries show intact acetylcholine- and sodium nitroprusside-induced vasodilation, suggesting that IAA preserves endothelial and smooth muscle function, respectively. IAA treatment also prevents arterial remodeling, oxidative stress, and kidney dysfunction in HSD DSS rats. Overall, our study identifies IAA as the first-in-class dual-action inhibitor of ETRs and ECE-1, which produces profound antihypertensive effect in vivo. IAA could also be therapeutically useful for other cardiovascular diseases in which ET-1 signaling is implicated.

The effect of robust coffee towards the malondialdehyde level in healthy adults

Coffee contains more than a thousand molecules, including phenolic compounds, vitamins, minerals and alkaloids. Caffeine, cafestol, kahweol and chlorogenic acid are related to lipid metabolism and can affect serum lipid profiles. Clinical studies have reported the effects of caffeine on cardiac arrhythmias, liver function, serum cholesterol and blood pressure. Malondialdehyde (MDA) in the human body is a by-product of free radicals (oxidative stress), which can indicate whether oxidative stress is detrimental. This study aims to analyse the effect of strong coffee on MDA levels in healthy adults. This study used a quasi-experimental design with a nonequivalent control group. This design was divided into two groups: the treatment group and the control group. The treatment group was given the treatment of drinking coffee and not eating foods that can raise cholesterol. In the control group, they did not drink coffee or eat foods that could cause increased malondialdehyde levels. The results showed that coffee increased MDA levels in 91% of the samples. Thus, strong coffee can increase malondialdehyde (MDA) levels in healthy adults.

Indices of Inflammation, Oxidative Stress and DNA damage in T2DM patients with and without Insulin Therapy

Background: Type 2 Diabetes Mellitus is a metabolic disorder associated with excessive free radical generation and oxidative stress. Pharmacological interventions of T2DM targets on glycemic control and reduce the circulatory levels of oxidative stress and inflammation. Aim: The study compared the levels of oxidative stress, inflammation and the extent of DNA damage in T2DM patients undergoing different treatment modalities. Methods: 150 subjects recruited for this study belonged to the age group of 35-65 years. Participants were grouped as healthy controls (n=50), diabetics treated with oral hypoglycemic agent metformin (n=50) and diabetics undergoing combined therapy of insulin and metformin (n = 50). All the participants underwent the assessment of anthropometric measures, baseline blood pressure and blood samples were analysed for FBS, HbA1c, MDA, TAC, Hs-CRP and DNA damage. Results: Analysis using one-way ANOVA showed that despite the same age and duration of T2DM, patients in insulin therapy group had significantly higher levels of oxidative stress, inflammation and DNA damage when compared to T2DM patients treated with metformin alone. Further, significant correlations were observed for the above parameters with the duration of T2DM.Conclusion: The study concludes that oxidative stress, systemic inflammation and cellular senescence are more prominent in T2DM patients undergoing insulin therapy. Poor glycemic control observed in these patients could be attributed to increased insulin resistance as a consequence of oxidative stress and inflammation.

Amelioration of lipopeptide biosurfactants for enhanced antibacterial and biocompatibility through molecular antioxidant property by methoxy and carboxyl moieties

Biosurfactants having surface-active biomolecules have been the cynosure in environment research due to their vast application. However, the lack of information about their low-cost production and detailed mechanistic biocompatibility limits the applicability. The study explores techniques for the production and design of low-cost, biodegradable, and non-toxic biosurfactants from Brevibacterium casei strain LS14 and excavates the mechanistic details of their biomedical properties like antibacterial effects and biocompatibility. Taguchi’s design of experiment was used to optimize for enhancing biosurfactant production by optimal factor combinations like Waste glycerol (1%v/v), peptone (1%w/v), NaCl 0.4% (w/v), and pH 6. Under optimal conditions, the purified biosurfactant reduced the surface tension to 35 mN/m from 72.8 mN/m (MSM) and a critical micelle concentration of 25 mg/ml was achieved. Spectroscopic analyses of the purified biosurfactant using Nuclear Magnetic Resonance suggested it as a lipopeptide biosurfactant. The evaluation of mechanistic antibacterial, antiradical, antiproliferative, and cellular effects indicated the efficient antibacterial activity (against Pseudomonas aeruginosa) of biosurfactants due to free radical scavenging activity and oxidative stress. Moreover, the cellular cytotoxicity was estimated by MTT and other cellular assays revealing the phenomenon as the dose-dependent induction of apoptosis due to free radical scavenging with an LC50 of 55.6 ± 2.3 mg/ml.

BGP-15 Protects against Doxorubicin-Induced Cell Toxicity via Enhanced Mitochondrial Function

Doxorubicin (DOX) is an efficacious and commonly used chemotherapeutic agent. However, its clinical use is limited due to dose-dependent cardiotoxicity. Several mechanisms have been proposed to play a role in DOX-induced cardiotoxicity, such as free radical generation, oxidative stress, mitochondrial dysfunction, altered apoptosis, and autophagy dysregulation. BGP-15 has a wide range of cytoprotective effects, including mitochondrial protection, but up to now, there is no information about any of its beneficial effects on DOX-induced cardiotoxicity. In this study, we investigated whether the protective effects of BGP-15 pretreatment are predominantly via preserving mitochondrial function, reducing mitochondrial ROS production, and if it has an influence on autophagy processes. H9c2 cardiomyocytes were pretreated with 50 μM of BGP-15 prior to different concentrations (0.1; 1; 3 μM) of DOX exposure. We found that BGP-15 pretreatment significantly improved the cell viability after 12 and 24 h DOX exposure. BGP-15 ameliorated lactate dehydrogenase (LDH) release and cell apoptosis induced by DOX. Additionally, BGP-15 pretreatment attenuated the level of mitochondrial oxidative stress and the loss of mitochondrial membrane potential. Moreover, BGP-15 further slightly modulated the autophagic flux, which was measurably decreased by DOX treatment. Hence, our findings clearly revealed that BGP-15 might be a promising agent for alleviating the cardiotoxicity of DOX. This critical mechanism appears to be given by the protective effect of BGP-15 on mitochondria.

Mechanism of spinal cord injury regeneration and the effect of human neural stem cells-secretome treatment in rat model.

Globally, complete neurological recovery of spinal cord injury (SCI) is still less than 1%, and 90% experience permanent disability. The key issue is that a pharmacological neuroprotective-neuroregenerative agent and SCI regeneration mechanism have not been found. The secretomes of stem cell are an emerging neurotrophic agent, but the effect of human neural stem cells (HNSCs) secretome on SCI is still unclear. To investigate the regeneration mechanism of SCI and neuroprotective-neuroregenerative effects of HNSCs-secretome on subacute SCI post-laminectomy in rats. An experimental study was conducted with 45 Rattus norvegicus, divided into 15 normal, 15 control (10 mL physiologic saline), and 15 treatment (30 μL HNSCs-secretome, intrathecal T10, three days post-traumatic). Locomotor function was evaluated weekly by blinded evaluators. Fifty-six days post-injury, specimens were collected, and spinal cord lesion, free radical oxidative stress (F2-Isoprostanes), nuclear factor-kappa B (NF-κB), matrix metallopeptidase 9 (MMP9), tumor necrosis factor-alpha (TNF-α), interleukin-10 (IL-10), transforming growth factor-beta (TGF-β), vascular endothelial growth factor (VEGF), B cell lymphoma-2 (Bcl-2), nestin, brain-derived neurotrophic factor (BDNF), glial cell line-derived neurotrophic factor (GDNF) were analyzed. The SCI regeneration mechanism was analyzed using partial least squares structural equation modeling (PLS SEM). HNSCs-secretome significantly improved locomotor recovery according to Basso, Beattie, Bresnahan (BBB) scores and increased neurogenesis (nestin, BDNF, and GDNF), neuroangiogenesis (VEGF), anti-apoptotic (Bcl-2), anti-inflammatory (IL-10 and TGF-β), but decreased pro-inflammatory (NF-κB, MMP9, TNF-α), F2-Isoprostanes, and spinal cord lesion size. The SCI regeneration mechanism is valid by analyzed outer model, inner model, and hypothesis testing in PLS SEM, started with pro-inflammation followed by anti-inflammation, anti-apoptotic, neuroangiogenesis, neurogenesis, and locomotor function. HNSCs-secretome as a potential neuroprotective-neuroregenerative agent for the treatment of SCI and uncover the SCI regeneration mechanism.

The physiological role of green tea catechins

Green tea is one of the most popular drinks consumed in the world. Important components contained in green tea and having antioxidant and anticarcinogenic properties are catechins - organic substances belonging to the class of polyphenolic compounds. Green tea contains 4 main catechins: (-)-epicatechin, (-)-epicatechin-3-gallate, (-)-epigallocatechin and (-)-epigallocatechin-3-gallate. This review summarizes the results of key studies, predominantly performed over the last 5 years, which provide evidence that catechins in green tea protect against ultraviolet radiation, can improve the quality of life of patients suffering from cancer, cardiovascular, neurodegenerative, viral, infectious diseases, obesity and a number of other pathologies, as well as serve as a measure for the prevention of these diseases in healthy individuals. The most potent catechin found in green tea has been shown to be (-)-epigallocatechin-3-gallate. The anticarcinogenic effects of (-)-epigallocatechin-3-gallate in the case of prostate cancer, breast cancer, colorectal cancer are presented. The powerful antioxidant activity of catechins can form the basis for the prevention of the development of infectious and viral diseases, as well as improve the quality of life of patients with metabolic syndrome and obesity. Thus, green tea is not only a tonic drink, but also an important tool for the prevention and treatment of human diseases, in the pathogenesis of which free radical oxidation and oxidative stress play an important role. The areas of practical application of green tea catechins can be the treatment of malignant tumors (during a course of chemotherapy or radiation therapy), the treatment of viral, infectious and cardiovascular diseases, skin protection from ultraviolet rays, etc.

Ternary Inclusion Complex of Sinapic Acid with Hydroxypropyl-β-cyclodextrin and Hydrophilic Polymer Prepared by Microwave Technology

Sinapic acid (SA) is a poorly water-soluble substance which could result in poor bioavailability. The aim of this study was to determine the “hydroxypropyl β-cyclodextrin (HPβCD)” solubilization of SA in the presence of the auxiliary substance hydroxypropyl methylcellulose (HPMC) and to evaluate the ternary inclusion complex prepared by microwave technology. Phase-solubility profiles showed that HPβCD exhibited the greatest solubilizing effect on SA in the presence of HPMC. The enhanced rate of SA dissolution was exhibited by a ternary complex. Outcomes of analyses such as “DSC, FTIR, NMR, and SEM” confirmed the embedding of SA into the cavity of the HPβCD and the formation of a ternary inclusion complex. The outcomes of antioxidant activity (ABTS and nitric oxide scavenging activity) demonstrated that SA ternary inclusion complex (TIC) presented strong antioxidant activity, which might be a result of the enhanced solubility of SA in the TIC prepared by microwave technology. Hence, SA-TIC formulation could be a better dosage form which may protect the body from free radical damage and oxidative stress. Microwave technology greatly boosted the interaction of SA with HPβCD and HPMC, and such findings are expected to contribute to raising the solubility of SA, thereby improving the bioavailability of SA.

Various Fractions of Alcoholic Extracts from Dendrobium nobile Functionalized Antioxidation and Antiaging in D-Galactose-Induced Aging Mice.

The theory of free radical oxidative stress (ROS) is one of the leading theories of ageing, and antioxidants play an important role in antiaging. Dendrobium has always been popular as a natural antioxidant. This study investigated the effects of various polarity fractions of ethanol extracts from Dendrobium nobile Lindl. (D. nobile) on D-galactose-induced aging mice. D. nobile stems were extracted by ethanol to form the crude extract (EA), which was sequentially extracted by trichloromethane, ethyl acetate, and n-butanol to yield the secondary extracts, named TCM, EAC, and NBA, respectively. EA, TCM, EAC and NBA were intragastrically administered at a dose of 200 mg/kg b.w. to the aging mice induced by D-galactose for 8 weeks. Compared with the aging control group (AC), D. nobile extracts reduced body weight and lipid accumulation and enhanced endurance and immunity by increasing the index of the spleens and thymus. Meanwhile, D. nobile extracts showed antioxidant properties by lowering Malondialdehyde (MDA) levels and increasing the activities of superoxide dismutase (SOD), catalase (CAT), and Glutathione peroxidase (GSH-Px) in the skin, blood, liver, and brain. Furthermore, D. nobile extracts had a good protective effect on the cell structure and function against lesions of the skin, liver, brain, kidney, and ovary of aging mice. In particular, EA and EAC had better antioxidant and antiaging effects, suggesting that the most effective components were flavonoids and polyphenols that existed in EAC. Both EA and EAC downregulated the expression of aging-related genes such as Il1a, Il1b, Il1rn, Ccl3, Ccl4, Fos and Gck in the brain at the transcriptome level. Both EA and EAC reversed the increase in the Firmicutes/Bacteroidota ratio in aging mice, increased the abundance of probiotic bacteria Lactobacillus and Muribaculum, and decreased the abundance of pathogenic bacteria such as Staphylococcus, Corynebacterium and Brevibacterium. The EA and EAC extracts of D. nobile have better effects on immunity improvement, antioxidation and antiaging by remodelling the intestinal microecosystem and downregulating the expression of age-promoting genes in the brain. D. nobile, especially EA and EAC extracts, could be used as an antiaging drug or functional food.

Preclinical studies on melanogenesis proteins using a resveratrol-nanoformula as a skin whitener

A naturally occurring polyphenol called trans-resveratrol has received a lot of attention due to its possible health advantages for humans. The low solubility of trans-resveratrol and its isomerization upon UV exposure strongly limit its application as a skin-whitening agent. In the present study, to increase trans-resveratrol solubility, a new nanoformula was created by combining hydrophilic surfactants and oils. Trans-Resveratrol nanoformula has been prepared, characterized, and applied as a skin-whitening agent on the dorsal skin of Guinea pigs. The optimized trans-resveratrol nanoformula with a particle size of 63.49 nm displayed a single peak and a polydispersity index [0.36 ± 0.02]. In addition, the zeta potential of the optimized formula was −30.4 mV, confirming the high stability of this nanoformula. The melanin contents in the trans-resveratrol nanoformula-treated group were substantially lower than those of the control and the blank nanoformula-treated groups after staining of the dorsal skins [black areas] of guinea pigs with Fontana Mountain dye. The pigmentation index in the control, blank nanoformula, and optimized trans-resveratrol nanoformula were 329.4 ± 36.9, 335.8 ± 71.4, and 124.8 ± 19.6 respectively. Confirming this finding, immunohistochemistry analysis of skin tissues revealed that the expressions of melanogenesis-regulating proteins such as tyrosinase and microphthalmia-associated transcription factor were down-regulated. The safety of topical application of trans-resveratrol nanoformula was validated by no changes in free radical levels and oxidative stress markers proteins in the livers and kidneys of guinea pigs at the end of the experiment. Conclusions: A novel trans-resveratrol nanoformula as well as the mechanism whereby it promotes skin whitening effects were presented. Furthermore, the study illustrated that trans-resveratrol nanoformula is safe, non-toxic, and can be applied for skin whitening, although more research on human skin is needed.

Hepatoprotective Effect of Ethanolic Extract of Garlic Against Reserpine Induced Toxicity in Wistar Rats.

Reserpine, a bioactive compound isolated from the roots of Rauwolfia serpentine, is known to deplete dopamine, a neurotransmitter. The clinical application of reserpine has been associated to manage hypertension, insanity, insomnia and schizophrenia. However, the usage of reserpine as a drug is restricted because of its ability of inducing excess free radicals production and oxidative stress resulting into damage to liver and other organs. Here, we have explored the antioxidative potential of extract of garlic prepared using ethanol (EEG) against reserpine-induced hepatic damage in the albino Wister rats.The animals were divided intofour different groups containing 6 animals in each: (1) control + placebo, (2) control + EEG, (3) reserpine and (4) reserpine with EEG. The reserpine treatment resulted into sharp increase in the level of MDA and significant reduction in the activitiesof key antioxidative enzymes (SOD, GST, and CAT) in the rat liver. It also caused sharp perturbations in the levels of certain hepatic transaminases (ALT, AST) and glycolytic LDH. The histopathological results revealed hepatic necrosis, which could have occurred due to reserpine induced lipid peroxidation as well as reduction in the levels of antioxidant species.The administration of EEG, however, significantly ameliorated reserpine induced hepatotoxicity. These results reflected the ameliorative property of EEG, which was probably mediated via its antioxidant function as it contains several bioactive molecules with free radical quenching potential.This study suggestedthe prospective application of EEG as a supplement to combat the side effects of reserpine.

Ameliorative effects of Anchomanes difformis aqueous extract against oxidative stress in the testes and epididymis of streptozotocin-induced diabetic male Wistar rats

Hyperglycemia is a central trait of diabetes mellitus (DM) and is linked to an increase in free radical generation and oxidative stress in the testes, resulting in testicular tissue damage and male infertility. Synthetic medicines are commonly used to manage diabetes; however, they are costly and associated with adverse effects. As a result, the search for a safer and affordable alternative from medicinal plants that contain antioxidants has become imperative to scavenge free radicals caused by hyperglycaemia, thereby alleviating male reproductive dysfunction. Therefore, the present aimed to investigate the ameliorative effects of Anchomanes difformis aqueous extract against oxidative stress in the testes and epididymis of streptozotocin-induced diabetic male Wistar rats. A total of 64 male Wistar rats (eight weeks old) weighing 180 ± 10 mg/kg were divided into seven groups at random. Type 2 diabetic mellitus (T2DM) was induced by streptozotocin (STZ) and a 10% fructose injection intraperitoneally using 40 mg/kg body weight rats. The levels of malondialdehyde (MDA), catalase (CAT), and superoxide dismutase (SOD) activity, reduced glutathione (GSH) concentration, and ferric reducing antioxidant (FRAP) as well as 2, 2-diphenyl-1-picrylhydrazyl (DPPH) values were used to establish the testicular oxidative status. It was found thatA.difformisextract significantly (p < 0.05) lowered MDA levels in diabetic rats. Both CAT and SOD activity were significantly (p < 0.05) lower following induction of DM and increased (p < 0.05) after treating withA. difformis. The findings of this study show that A. difformis extract could be a promising source of lead compounds for the development of a therapeutic agent to treat male infertility caused by DM complications.

Paraquat modulates immunological function in bone marrow-derived macrophages.

The herbicide paraquat (PQ) is known to affect the immune system. Many reports have indicated that PQ impacts on the viability and functions of the immune cells, however, the underlying mechanism in detail is still unknown. The aim of this study was to evaluate the effects of PQ on the free radical production, oxidative stress, cell death and pro-inflammatory gene expression of murine bone marrow-derived macrophages (BMDMs) from C57BL/6NJcl mice in vitro. BMDMs were incubated with PQ at 0, 200 and 400 µM concentrations for 24 h. Intracellular reactive oxygen species (ROS) production, apoptosis, cell viability, nitric oxide, inducible nitric oxide synthase (iNOS), and IL-6 expression levels were measured. The results revealed that PQ treatments led to a decrease in the cell viability and induced apoptotic cell death in a dose-dependent manner. Additionally, PQ also induced the generation of ROS. The mRNA level of the pro-inflammatory mediator genes iNOS and IL-6 were also elevated, while the level of lipid peroxide (malondialdehyde) production remained unaltered. Interestingly, the PQ treatment led to a decrease in the nitric oxide production. These results indicate that the increased cellular ROS production, due to the PQ treatment, induces apoptosis and the herbicide triggers production of iNOS and IL-6 in BMDMs.