Zingiberene exerts chemopreventive activity against 7,12-dimethylbenz(a)anthracene-induced breast cancer in Sprague-Dawley rats.

Breast cancer is the primary cause of cancer-related death in females, wherein increased mortality of breast cancer patients is recorded worldwide. Zingiberene is a monocyclic sesquiterpene from the ginger plant and has many pharmacological benefits. In this exploration, we assessed the anticancer actions of Zingiberene against the 7,12-dimethylbenz(a)anthracene (DMBA)-stimulated mammary carcinogenesis in rats and MDA-MB-231 cells. Breast cancer was induced in the Female Sprague-Dawley rats through the 25 mg/kg of DMBA in 0.5 ml of corn oil and then treated with 20 and 40 mg/kg of Zingiberene, respectively. The body weight of animals and tumor volume was measured. Hematological parameters, transaminases, lipid profile, lipid peroxidation, and antioxidants status were scrutinized using standard techniques. The estrogen receptor-α and inflammatory markers were inspected by using respective assay kits. Histological damage scores were determined. In vitro experiments were conducted to scrutinize Zingiberene's effect on cell viability and apoptotic cell death in MDA-MB-231 cells. Zingiberene substantially modulated the DMBA-stimulated physiological and hematological changes and decreased the transaminases, and lipid peroxidation in the DMBA-stimulated animals. Zingiberene also elevated the antioxidant level and suppressed the inflammatory markers. Histological study revealed the protective effects of Zingiberene. The viability of MDA-MB-231 cells was noticeably diminished by the Zingiberene, thus inducing apoptotic cell death. Overall, our findings reliably proved the anticancer potential of Zingiberene against the DMBA-stimulated mammary tumorigenesis, and it could be a promising chemotherapeutic agent.

Deteriorating insulin resistance due to WL15 peptide from cysteine and glycine-rich protein 2 in high glucose-induced rat skeletal muscle L6 cells.

This study investigates the antioxidant and antidiabetic activity of the WL15 peptide derived from Channa striatus on regulating the antioxidant property in the rat skeletal muscle cell line (L6) and enhancing glucose uptake via glucose metabolism. Increased oxidative stress plays a major role in the development of diabetes and its complications. Strategies are needed to mitigate the oxidative stress that can reduce these pathogenic processes. Our results showed that with treatment with WL15 peptide, the reactive oxygen species significantly decreased in L6 myotubes in a dose-dependent manner, and increased antioxidant enzymes help to prevent the formation of lipid peroxidation in L6 myotubes. The cytotoxicity of WL15 is evaluated in the L6 cells and found to be non-cytotoxic at the tested concentration. Also, for the analysis of glucose uptake activity in L6 cells, the 2-(N-[7-nitrobenz-2-oxa-1,3-diazol-4-yl]amino)-2-deoxy- d -glucose assay was performed in the presence of wortmannin and genistein inhibitors. WL15 demonstrated antidiabetic activities through a dose-dependent increase in glucose uptake (64%) and glycogen storage (7.8 mM). The optimal concentration for the maximum activity was found to be 50 µM. In addition, studies of gene expression in L6 myotubes demonstrated upregulation of antioxidant genes and genes involved in the pathway of insulin signaling. In cell-based assays, WL15 peptide decreased intracellular reactive oxygen species levels and demonstrated insulin mimic activity by enhancing the primary genes involved in the insulin signaling pathway by increased glucose uptake indicating that glucose transporter type 4 (GLUT4) is regulated from the intracellular pool to the plasma membrane.

Brucine promotes apoptosis in cervical cancer cells (ME-180) via suppression of inflammation and cell proliferation by regulating PI3K/AKT/mTOR signaling pathway.

Brucine are the main constituents of Strychnos nux-vomica. Earlier reports have determined brucine shows anti-inflammatory, analgesic and excellent anti-tumor drug. Even though its anticervical cancer cells remains not clearly evaluated. So that, we hypothesized the anti-cervical cancer activity of brucine against the cervical (ME-180) cells. Brucine inhibited the inflammation, cell proliferation and promoted rate of apoptotic cell death ad reduced the mitochondrial potential, which is evidenced by respective (AO/EB, Rh-123, and PI) staining. Furthermore ELISA and real time PCR reaction determined that brucine were down regulated inflammatory (TNF-α, NF-kB, IL-6 & COX-2) cell proliferation (Cyclin D1) and apoptotic marker Bax, caspase-3, PI3K (phosphoinosital 3 kinase), AKT, mTOR (mammalian target of rapamycin) and over expression Bcl-2, associated death promoter. These findings were confirmed and finally suggested that brucine inhibited inflammation, cell proliferation and promoted the apoptosis through the down-regulation of PI3K/AKT/mTOR pathway. Taken together, these data were exhibited brucine as a good therapeutic agents for the prevention of anticancer cervical cancer drugs.

Zinc oxide nanoparticles from Corydalis yanhusuo attenuated the mycoplasmal pneumonia in mice through inhibiting the MAPKs signaling pathway.

BACKGROUND: The Mycoplasma pneumoniae (M.pneumoniae) was accounted to 3-10% of total pneumonia incidences. In recent decades, metallic nanoparticles were extensively examined as nano-antibiotics. OBJECTIVE: In this investigation, we intended to inspect the therapeutic potential of Zinc oxide nanoparticles (ZnONPs) from (Corydalis yanhusuo) C. yanhusuo against the mycoplasma infected pneumonia in mice. METHODOLOGY: The ZnONPs were formulated via green route technique and characterized by UV-vis spectroscopy, transmission electron microscopy, Fourier transform infrared technique, and atomic force microscopy. The antimicrobial activity of formulated ZnONPs was tested by well diffusion method. The total protein, interleukin-1 (IL-1), interleukin-6 (IL-6), interleukin-8 (IL-8), tumor necrosis factor alpha (TNF-α) and transforming growth factor (TGF) status in the BALF of M. pneumonia infected animals were investigated via kit method. The expressions of ERK1/2, JNK1/2, and NF-κB were examined through the Western blotting. The Histopathological analysis of lung tissues of experimental animals was done. RESULTS: The UV-vis spectroscopy and TEM examinations were proved the existence of CY-ZnONPs. The formulated CY-ZnONPs were displayed the potential antimicrobial activity. The supplementation of CY-ZnONPs were noticeably diminished the total protein and IL-6, IL-8, and TNF-α levels in the BALF of pneumonia mice. The ERK1/2, JNK1/2, and NF-κB expressions were appreciably diminished in the CY-ZnONPs supplemented mice. It also reduced the inflammatory cells penetration, and exhibited normal tissue arrangements in the lung tissues of pneumonia mice. CONCLUSION: The findings of this investigation were proved that the synthesized CY-ZnONPs has the potential to ameliorate the M. pneumoniae infected pneumonia in investigational mice.

Nigericin Abrogates Maternal and Embryonic Oxidative Stress in the Streptozotocin-Induced Diabetic Pregnant Rats.

Hyperglycemic exposure in diabetic pregnancy can lead to many developmental changes, such as delayed development, fetal malformations, and fetal/embryo death. These detrimental complications are collectively known as diabetic embryopathy or teratogenesis. The current study focuses to discover the therapeutic properties of the nigericin against the STZ-stimulated diabetic embryopathy via alleviation of maternal and embryonic oxidative stress. The male and female rats at a 1:1 ratio were permitted to mate overnight to establish the course of pregnancy. The pregnant rats were distributed into four groups control, diabetic pregnant (via administering 40 mg/kg of STZ), and diabetic + 10 and 20 mg/kg of nigericin-administered (via oral gavage from days 5 to 12) groups, respectively. The glucose level, urine output, diet intake, and body weight were determined carefully. The embryo and placenta weight and implantation rates were examined, and data were tabulated. The total protein and lipid profiles were assessed using respective kits. The oxidative stress markers and antioxidant enzymes were examined using respective assay kits. The 10 and 20 mg/kg of nigericin treatment decreased the glucose level and urine output and improved the diet intake and body weight gain in diabetic pregnant rats. The nigericin also decreased the total protein, cholesterol, triglycerides, and very-low-density lipoprotein (VLDL) and improved the high-density lipoprotein (HDL) in the serum of pregnant rats. The levels of malondialdehyde (MDA), reactive oxygen species (ROS), and protein carbonyls were decreased by the nigericin in both liver and embryos of the pregnant rats. The levels of glutathione (GSH), total thiols, and activities of catalase (CAT), glutathione reductase (GR), superoxide dismutase (SOD), glutathione peroxidase (GPX), and glutathione S-transferase (GST) were improved by the nigericin in the diabetic pregnant rats. Altogether, these results provide evidence that nigericin treatment remarkably attenuates the diabetes-stimulated embryopathy in rats. The nigericin effectively decreased embryo lethality, reduced glucose and dyslipidemia, and relieves oxidative stress via upregulating the antioxidant enzyme activities. Hence, it can be a talented therapeutic agent to treat diabetic pregnancy-associated complications.

Benzo(A)Pyrene-Induced Lung Cancer: Chemo Protective Effect of Coronarin D in Swiss Albino Mice.

Lung cancer is considered one of the most prevalent cancers worldwide and also has a high death rate. The prevalence of lung cancer is high in developed countries than in developing countries due to the lifestyle changes and quality of air. Coronarin D is a diterpene, which is isolated from the Hedychium coronarium. It demonstrated several pharmacological properties such as anti-allergic, anti-inflammatory, antimicrobial, and anticancer activities. In the current investigation, the potential of Coronarin D on the B(a)P-induced lung cancer was studied in the experimental mice model. The B(a)P-administrated animals exhibited a reduced level of immune cells, IgG, IgM, immune complexes, SOD, and CAT. The B(a)P-administrated animals expressed high levels of IgA, LPO, xenobiotic markers, tissue marker, tumor marker, and proinflammatory cytokines. On treatment with Coronarin D, the level of neutrophils, lymphocytes, leucocytes, and absolute neutrophils was elevated in the B(a)P-administered mice. The immune complex was augmented in the Coronarin D-treated animals in comparison with B(a)P-treated mice. The level of IgG and IgM was increased, whereas the level of IgA was reduced in the Coronarin D-treated animals. The level of LPO was downregulated, whereas the level of SOD and CAT was upregulated in Coronarin D-treated animals. The expression level of xenobiotic markers, tissue marker, tumor marker, and proinflammatory cytokines was reduced in the Coronarin D-treated animals. The histopathological results revealed that lung tissues of Coronarin D-treated animals had less alveolar damage with decreased hyperplasia. These findings suggest that the Coronarin D can be utilized as a potent chemopreventive agent for treating lung cancer in the future.

Triptonide, a Diterpenoid Displayed Anti-Inflammation, Antinociceptive, and Anti-Asthmatic Efficacy in Ovalbumin-Induced Mouse Model.

The present study was intended to explore the valuable effects of triptonide on inflammation, asthmatic, and nociceptive. Triptonide possesses numerous beneficial effects extensively managed in the treatment of inflammation disease condition. Initially, triptonide showed anti-inflammation properties over lipopolysaccharide-induced RAW 264.7 cells. Hence, the present study was directed to explore the protecting efficacy of triptonide in ovalbumin (OVA)-induced asthma in mice. Asthma was induced intraperitoneally administration (200µL) in female BALB/c mice with suspension which has ovalbumin (100 µg/mL) and aluminum hydroxide (10 mg/mL). Triptonide (30 mg/kg) over OVA-induced experimental animals altered lung mass, nitric oxide, myeloperoxidase, immunoglobulin E status, interleukins (4, 5, and 13) inflammatory cytokines status, and histological modifications. Animals were also managed with the standard drug dexamethasone (50 mg/kg) followed by the asthma induction, which is also efficient over OVA-induced experimental animals. The nociception was provoked in male Swiss mice by various chemicals (acetic acid, capsaicin, and glutamate). The animals were administered with triptonide (5, 10, and 15 mg/kg) and separate standard drugs like diclofenac sodium (10 mg/kg) and morphine (5 mg/kg) over chemical-induced nociceptive animals. The present outcome evidently established that the triptonide considerably reduced the various chemical-induced nociception in mice (Fig. 7A, B, and C). Ultimately, the present work explored the evident powerful anti-inflammation, antinociceptive, and anti-asthma properties of a diterpenoid, triptonide experimental animal models. And it is recommended that triptonide is an excellent compound in the management of asthma and its related diseases.

Anticancer Effect of Ruscogenin in B(a)P-Induced Lung Cancer in Mice via Modulation of Proinflammatory Cytokines and Mitochondrial Enzymes.

Lung cancer, one of the most often diagnosed malignancies, is the top cause of death in both men and women globally. In both developed and emerging countries, high incidences of cancer are becoming a huge health burden. Natural resources, including plants, have always been a possible source of lead compounds in the identification of optimal medications for cancer treatment, with natural resources accounting for around half of all anticancer drugs. Ruscogenin, a natural saponin, is a major component of Radix Ophiopogon japonicus with a well-established anticancer activity. In this study, the anticancer potential of ruscogenin against a B(a)P-challenged lung cancer model in mice was assessed. The mice were categorized into four groups: group I was as the control group, group II mice were challenged with B(a)P, group III rodents were treated with ruscogenin prior to challenge with B(a)P, and group IV rodents were treated with ruscogenin after B(a)P administration. Tumor incidence was calculated, and the following parameters were analyzed: body weight, lung weight, immunoglobulin (Ig) levels (IgG, IgA, and IgM), key marker enzymes, and proinflammatory cytokines in both treated and control mice. Lung tissues were analyzed via histopathological analysis. According to our results, all the markers that favor the growth of cancer were increased in the lung cancer group. After administration of ruscogenin, all the markers returned to their original levels, revealing the anticancer potential of ruscogenin.

Anti-atherosclerotic Effects of Myrtenal in High-Fat Diet-Induced Atherosclerosis in Rats.

The major cause of death worldwide is atherosclerosis-related cardiovascular disease (ACD). Myrtenal was studied to determine control rats were given standard diets and a high-fat diet was given to AS model groups. Atherosclerosis-related cardiovascular disease (ACD) is globally attributed to being a predominant cause of mortality. While the beneficial effects of Myrtenal, the monoterpene from natural compounds, are increasingly being acknowledged, its anti-atherosclerotic activity has not been demonstrated clearly. The present study is proposed to determine the anti-atherosclerotic activity of Myrtenal in high-fat diet-induced atherosclerosis (AS) rat models. Control groups were maintained with standard diets, the AS model rats were provided a high-fat diet, two of the experimental groups fed with a high-fat diet were treated with Myrtenal (50 mg/kg and 100 mg/kg), and one experimental group on high-fat diet was treated with simvastatin (10 mg/kg) for 30 days. The levels of inflammatory cytokines were analyzed using kits. The lipoproteins and the lipid profile were estimated using an auto-analyzer. The atherogenic index and marker enzyme activities were also determined. Serum concentrations of 6-keto-prostaglandin F1α (6-keto-PGF1α), thromboxaneB2 (TXB2), endothelin (ET), and nitric oxide (NO) were measured. The AS model groups indicated altered lipid profile, lipoprotein content, atherogenic index, calcium levels, HMG-CoA reductase activity, collagen level, and mild mineralization indicating atherosclerosis, while the AS-induced Myrtenal-treated groups demonstrated anti-atherogenic activity. The Myrtenal-treated groups exhibited a decreased TC, TG, and LDLc levels; increased HDLc levels; and a decline in the inflammatory cytokines such as CRP, IL-1ß, IL-8, and IL-18 when compared to the untreated AS rats. Furthermore, Myrtenal decreased ET, TXB2, and 6-keto-PGF1α levels indicating its anti-atherosclerotic activity. The study results thus indicate that Myrtenal modulates the lipid metabolic pathway to exert its anti-atherosclerotic activity.

Wound Healing Efficacy of Rosuvastatin Transethosomal Gel, I Optimal Optimization, Histological and In Vivo Evaluation.

This study aimed to make a formulation and statistical optimization of transethosomal formulations of rosuvastatin (ROS) to enhance its topical wound healing efficiency. Design-Expert® software was used to employ I optimal design. The formulation variables in the study were surfactant concentration (%w/v), ethanol concentration (%w/v) and surfactant type (span 60 or tween 80), while the dependent responses were entrapment efficiency percent (EE%), vesicle size (VS) and zeta potential (ZP). The numerical optimization process employed by the design expert software resulted in an optimum formula composed of 0.819439 (%w/v) span 60, 40 (%w/v) ethanol and 100 mg lecithin with a desirability of 0.745. It showed a predicted EE% value of 66.5517 vs. 277.703 nm and a ZP of -33. When it was prepared and validated, it showed less than a 5% deviation from the predicted values. The optimum formula was subjected to further characterizations, such as DSC, XRD, TEM, in vitro release, the effect of aging and wound healing efficiency. The DSC thermogram made a confirmation of the compatibility of ROS with the ingredients used in the formulation. XRD showed the encapsulation of ROS in the transethosomal vesicles. The TEM image pointed out the spherical nature of the nanovesicles with the absence of aggregation. Additionally, the optimum formula revealed an enhancement of drug release in comparison with the drug suspension. It also showed good stability for one month. Furthermore, it revealed good wound healing efficiency when compared with the standard silver sulphadiazine (1% w/w) ointment or the drug-loaded gel, which could be related to the enhanced penetration of the nanosized vesicles of TESMs into the skin, which enhances the wound healing process. So, it could be regarded as a promising carrier of ROS for the treatment of chronic wounds.

Sulfation of chitosan from Sepia kobiensis as potential anticoagulant and antibacterial molecule.

The present work aimed to synthesis of chitin, chitosan and sulfation of chitosan from cuttlebone of cuttlefish Sepia kobiensis. Principally chitin was extracted through sequential processes of demineralisation and deproteinzation. Then chitosan was synthesized by a deacetylation and finally sulfated at semi-heterogeneous condition using chlorosulfonic acid in N,N-dimethylformamide. The synthesized macromolecules were characterized for its structural, physical and thermal (CHN, DDA, FT-IR, NMR, XRD, Viscometric analysis, SEM and DSC) properties. Apart from anticoagulant potential of the sulfated chitosan was tested using human plasma by means of activated partial thromboplastin time (APTT) and prothrombin time (PT). Further sulfated chitosan was tested for antibacterial potential by well diffusion method against eleven human pathogenic clinical isolates of both Gram positive and Gram-negative strains and minimum inhibitory concentrations (MIC) was calculated accordingly. The results of this study revealed the effectiveness of the sulfated chitosan at semi-heterogeneous conditions as a potent antibacterial and anticoagulant molecule.

Biosynthesized Gold Nanoparticles Integrated Ointment Base for Repellent Activity Against Aedes aegypti L.

The present study focused on preparing a nano-ointment base integrated with biogenic gold nanoparticles from Artemisia vulgaris L. leaf extract. As prepared, nano-ointment was characterized by using Fourier-transform infrared spectroscopy, and the morphology of the nano-ointment was confirmed through a scanning electron microscope. Initially, the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide results showed nano-ointment cytocompatibility at different concentrations (20-200 µg/mL) against L929 cells. The in vitro hemolysis assay also revealed that the nano-ointment is biocompatible. Further studies confirmed that nano-ointment has repellent activity with various concentrations (12.5, 25, 50, 75, and 100 ppm). At 100 ppm concentration, the highest repellent activity was observed at 60-min protection time against the Aedes aegypti L. female mosquitoes. The results indicated that the increasing concentration of nano-ointment prolongs the protection time. Moreover, the outcome of this study provides an alternative nano-ointment to synthetic repellent and insecticides after successful clinical trials. It could be an eco-friendly, safer nano-bio repellent, which can protect from dengue fever mosquitoes.

Zinc oxide nanoparticles from Cassia auriculata flowers showed the potent antimicrobial and in vitro anticancer activity against the osteosarcoma MG-63 cells.

Osteosarcoma (OS) is a foremost mesenchymal bone neoplasm and it can occur at any age with survival rate is nearly 2-8 times lesser in elders than in teenagers. The clinical therapies for cancer treatment have gradually becoming outdated because of the developments of nano-medicine and multi-targeted drug-delivery. In this work, we green synthesized the zinc oxide nanoparticles from the Cassia auriculata flower (AS-ZnONPs) extract and evaluated its antimicrobial and in vitro anticancer potential against the OS MG-63 cells. The synthesized AS-ZnONPs were confirmed and characterized by using UV-vis spectroscopy, XRD, FE-SEM, and photoluminescence techniques. The antimicrobial activity of AS-ZnONPs was studied by disc diffusion technique. The viability of AS-ZnONPs treated MG-63 cells were examined by MTT assay. The apoptotic cells in the AS-ZnONPs treated MG-63 cells were assayed by dual staining. The MMP status of AS-ZnONPs treated cells were tested by Rh-123 staining. The cell adhesion assay was performed to detect the anticancer effects of AS-ZnONPs against MG-63 cells. The results of UV-vis spectroscopy, XRD, FE-SEM, and photoluminescence techniques proved the formation of AS-ZnONPs and it has the hexagonal wurtzite structures. AS-ZnONPs displayed the potent antimicrobial activity against the tested microbial strains. The AS-ZnONPs were appreciably inhibited the cell viability of MG-63 cells. The outcomes of fluorescence staining proved that AS-ZnONPs reduced the MMP and prompted the apoptosis in MG-63 cells. In conclusion, our discoveries demonstrated that the formulated AS-ZnONPs has the potent antimicrobial and in vitro anticancer activity against the MG-63 cells. The AS-ZnONPs could be potent chemotherapeutic agent in the future to treat the OS.

Cardioprotective properties of natural medicine in isoproterenol induced myocardial damage in the male Albino rats.

The main aim of this study is to investigate cardioprotective properties of natural medicine inmyocardial damage induced male Albino rats. The aqueous extractof Allium sativumwas used for the determination of phenolic compounds and flavonoids. The amount of phenol (1.39 ± 0.37 GAE/g dry weight) and flavonoids (49.1 ± 2.79 QE/g dry weight) were high in aqueous extract. A. sativumextract and showed 68.39 ± 3.6% DPPHscavenging activity. Isoproterenol was used to induce myocardial injury in Albino rats in vivo by subcutaneous injection (100 mg/kg body weight). To achieve this, experimental animals were categorized into six groups (n = 4), namely, positive, negative control, only isoproterenol administered groups, and garlic extract administered group at 100-300 mg extract/kg body weight. Oxidative stress marker and cardiac markers were assayed to analyze the cardioprotective properties of garlic extract. At 300 mg/kg doseof garlic extract, rat was recovered from various altered factors such as, aspartate aminotransferase, alkaline transminase and alkaline phosphatase. The rats treated with 300 mggarlic extract/kg body weight decreased the level of asparate aminotransferase (126 ± 6.4 IU/L) than other lower doses (100 mg extract/kg and 200 mg extract/kg). Alkaline transaminase level of rat serum level was 81 ± 4.34 IU/L. In the isoproterenol treated rats elevated level was observed (152 ± 4.42 IU/L enzyme activity). Pre-treatment of Albino rat with A. sativum extract reduced cardiac damage. Isoproterenol exposed animal showed 207.6 ± 1.2 mg/dL triglyceride and the garlic administered rat (300 mgextract/kg) reduced LDL-cholesterol level (61.3 ± 1.3 mg/dL) significantly (p < 0.05). Creatinine kinase -MB level was 269.5 ± 12.5 IU/L in the control animal and stress induced animal showed elevated level (572.3 ± 19.4 IU/L). Garlic treated experimental animal (300 µg/kg bw) decreased CK-MB level. To conclude, the aqueous extract of A. sativumshowed cardio protective properties against myocardial injury.

Troxerutin Abrogates Ischemic/Reperfusion-Induced Brain Injury through Ameliorating Oxidative Stress and Neuronal Inflammation by Inhibiting the Expression of NLRP3 in Sprague Dawley Rats.

Cerebral ischemic reperfusion (I/R) infarction is mostly associated with serious brain injury, cognitive damage, and neurological deficits. The oxidative stress mechanisms in the neurological region lead to higher reactive oxygen species production followed by oxidative stress, inflammation of neurons, and death of brain cells. The current work aims to evaluate the effect of troxerutin (TXN) on cerebral injury stimulated by I/R-induced ischemic stroke and examines the mechanistic effect of TXN on neuroinflammation in the Sprague Dawley model. The experimental rats were randomized in to four groups: (i) sham control, (ii) I/R + vehicle, (iii) I/R + 10 mg/kg bw TXN, and (iv) I/R + 20 mg/kg bw TXN. In the TXN administration and control, groups were injected intraperitoneally 15 min before reperfusion and every day for 7 days, except the sham group. Orally administered TXN (10 and 20 mg/kg/bw) modulated the water content, lowered the infarct volume, and abrogated score defects of neuron and changes in the brain tissue sample. In our study, the TXN-stimulated cerebral injury exhibited leakage of thiobarbituric acid reactive substances (TBARS), lipid hydroperoxides (LOOH) of the neuronal sample of tissues and showed higher antioxidant enzymes superoxide dismutase, catalase, the oxidized form of glutathione peroxidase, and the reduced form of glutathione levels. This biochemical result was additionally proved by histopathological assessment. Changes were made in antioxidant and inflammatory markers expressions interleukin-6 (IL-6), IL-4, IL-10, vascular endothelial growth factor, and cerebral induced rats. The overall findings showed that TXN protected the brain tissues from neuroinflammatory oxidative stress by reducing cerebral injury in Sprague Dawley rats. Further, the messenger RNA expression of cerebral I/R-induced animal tissues down-regulated NLRP3, caspase-1, tumor necrosis factor-α, ASC, IL-1ß, and Toll-like receptor 3 (TLR3). Therefore, the TXN action on TLR3 induced brain stroke is an excellent therapeutic approach for brain damage.