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Objective: The most prevalent brain‐specific microRNA, MicroRNA‐124, exhibits anti‐inflammatory properties. Luteolin nano‐formulation with Zn oxide in the form of L/ZnO NPs may boost anti‐diabetic properties; however, its beneficial effect on miRNAs is yet unknown in diabetes. The effectiveness of L/ZnONPs supplements in preventing diabetic neurodegeneration by modulating inflammatory responses in a diabetic model was investigated. Methods: A diabetic rat model was induced by a high‐fat diet and streptozotocin (30 mg/kg I.P.). Plasma glucose, insulin, and HOMR‐IR levels, as well as cytokines, lipid peroxidation, GSH/GSSG, and glucose transporter 1, were determined along with the tight junction proteins occludin (OCLN) and zona occludens 1 (ZO‐1). Moreover, the expressions of brain CCAAT/enhancer‐binding protein (C/EBPA mRNA), miR‐124, glial fibrillary acidic protein (GFAP), and NF‐kBp65 were measured alongside the histological investigation. Results: The results revealed that L/ZnO NPs were able to diminish lipid peroxidation, increase the activity of antioxidant enzymes, and reduce inflammation under oxidative stress. Consequently, it was able to reduce hyperglycemia, elevate insulin levels, and improve insulin resistance. Besides, L/ZnO NPs upregulate miR‐124, reduce C/EBPA mRNA, increase BCl‐2, and inhibit apoptosis. The results indicate that diabetes raises BBB permeability via tight junction protein decline, which is restored following L/ZnO NPs treatment. Luteolin/ZnO NPs regulate miR‐124 and microglia polarization by targeting C/EBPA and are expected to alleviate inflammatory injury via modulation of the redox‐sensitive signal transduction pathways. Luteolin/ZnO NPs have a novel target for the protection of the BBB and the prevention of neurological complications in diabetes. [ABSTRACT FROM AUTHOR]

Probiotics have been suggested as a safe and cost-effective approach to prevent or treat hepatocellular carcinoma (HCC). Some of the exopolysaccharides (EPSs) produced by lactic acid bacteria confer health benefits such as immunomodulatory and antitumor activities. The present study was therefore aimed to investigate the immunomodulatory effect of Lactobacillus acidophilus ATCC 4356 EPSs against diethylnitrosamine (DEN) and gamma radiation (IR) induced HCC either as prevention or treatment in male rats' model. Biochemical results revealed a significant increase in serum ALT and γ-GT activities as well as MDA, IL-17, TGF-β1, signal transducer and activator of transcription-3 protein (STAT3), mitogen-activated protein kinase p38 (p38MAPK) levels in the liver tissue. The gene expression level of the liver toll-like receptor 2 (TLR-2) gene was also increased. However, prevention and treatment with EPSs ameliorated most of the investigated parameters. The histopathological observations of liver tissues were in agreement with restored biochemical results. In conclusion, Lactobacillus acidophilus ATCC 4356 EPSs are efficacious control against HCC throughout the regulation of TLR2/STAT-3/P38-MAPK Pathway associated with inflammation. Therefore, our novel EPSs ATCC 4356 could be used as a good, safe and effective probiotic to prevent hepatocarcinogenesis in suspected patients. [ABSTRACT FROM AUTHOR]

Cancer is a mortality contributor worldwide, and breast cancer is the most common among women. Despite the numerous breast cancer therapeutic strategies, they either have limitations or sometimes are resisted by cancer, so new approaches are needed to tackle those restrictions. Nanotechnology offers exciting leaps in the diagnosis and treatment of cancer, especially breast cancer. The main objective of this study was to investigate the effect of the newly synthesized gallium nanoparticles coated by Ellagic acid (EA-GaNPs) on the induced mammary gland carcinogenesis in female rats and their antibacterial activities comparison with standard antibiotics (Ketoconazole (100 μg/ml) and Gentamycin (4 μg/ml)) by disc diffusion method using eight different microbial species. The antitumor efficacy of EA-GaNPs was conducted both in vitro and in in vivo. The result of antimicrobial activity of EA-Ga NPs (1 mg/1 mL) revealed moderate toxicity behavior against Gram-positive {Staphylococcus aureus, Bacillus subtilis, Bacillus cereus) and Gram-negative pathogenic bacteria {Escherichia coli, Proteus vulgarfs) also, antifungal activity was detected against {Aspergillus terreus). In vitro study showed that EAGaNPs inhibited human breast cancer cell line (MCF-7) proliferation with IC50 of 2.86 μg/ml. Although in vivo; the administration of EAGaNPs to DMBA-treated rats ameliorated the hyperplastic state of mammary gland carcinogenesis induced by DMBA. Additionally, EAGaNPs administration significantly modulated the activities of ALT and AST, as well as the levels of urea and creatinine in serum. Also, EA-GaNPs administration improved the antioxidant state by increasing Superoxide dismutase activity and GSH content, and decreasing malondialdehyde content in the mammary tissue, besides enhancing the apoptotic activity through elevating the levels of caspase-3 and decreasing the protein intensities of protein kinase B & phosphatidyl inositide 3-kinases. Furthermore, a significant decrease in serum Total iron-binding capacity accompanied by a significant increase in the level of calcium was noted. So, it can be concluded that the newly synthesized nanoparticles EA-GaNPs have an efficient antitumor activity that was manifested by reduction of the viability on the human breast cancer cell line (MCF-7) in vitro. Also, in vivo against the chemically induced mammary gland carcinogenesis in a female rat model. Histopathological findings were in harmony with biochemical and molecular results showing the effectiveness of EA-GaNPs against mammary carcinogenesis. Therefore, EA-GaNPs could be a promising, potent anti-cancer compound. [ABSTRACT FROM AUTHOR]

d‐Galactosamine (d‐GalN) is a well‐known toxin that causes many metabolic and morphological abnormalities resulting in advanced renal failure and liver damage. Occupational exposure to low‐level ionizing radiation (<1 Gy) was shown to enhance cell protection via attenuating an established inflammatory process. The present study was therefore aimed to investigate the protective impact of Amphora coffaeiformis extract and low dose gamma radiation against d‐GalN induced renal damage in rats. Forty‐eight adult male Swiss albino rats were distributed equally into eight groups. The measurements included antioxidants activities (superoxide dismutase, catalase and glutathione peroxidase) as well as lipid peroxidation level in kidney tissue. Also, kidney function tests and inflammatory markers (tumor necrosis factor alpha and nuclear factor kappa‐light‐chain‐enhancer of activated B cells) were measured. Additionally, relative quantification of kidney nuclear factor erythroid 2‐related factor 2 (Nrf‐2) gene was estimated. Histopathological examination was also performed in kidney tissue. The results revealed decreases in antioxidant activities and downregulation of Nrf‐2 expression accompanied by increases in lipid peroxidation level, kidney function tests and inflammatory markers in d‐GaIN group. The treatment with Amphora algal extract and low dose gamma radiation ameliorated the previous measurements which were harmony with histopathological findings. In conclusion, A coffaeiformis extract and low dose gamma radiation provided marked functional and histological effects in the treating acute renal damage induced by d‐GalN in rats. [ABSTRACT FROM AUTHOR]

β-glucans are one of the most abundant forms of polysaccharides known as biological response modifiers which influence host's biological response and stimulate immune system. Accordingly, this study was initiated to evaluate irradiated β-glucan as a modulator for cellular signaling growth factors involved in the pathogenesis of hepatocellular carcinoma in rats. Hepatocellular carcinoma was induced with 20 mg diethylnitrosamine/kg BW. Rats received daily by gastric gavage 65 mg irradiated β-glucan/kg BW. It was found that treatment of rats with diethylnitrosamine induced hepatic injury and caused significant increase in liver injury markers with a concomitant significant increase in both hepatic oxidative and inflammatory indices: alpha-fetoprotein, interferon gamma, and interleukin 6 in comparison with normal and irradiated β-glucan-treated groups. Western immunoblotting showed a significant increase in the signaling growth factors: extracellular signal-regulated kinase 1 and phosphoinositide 3-kinase proteins in a diethylnitrosamine-treated group while both preventive and therapeutic irradiated β-glucan treatments recorded significant improvement versus diethylnitrosamine group via the modulation of growth factors that encounters hepatic toxicity. The transcript levels of vascular endothelial growth factor A and inducible nitric oxide synthase genes were significantly higher in the diethylnitrosamine-treated group in comparison with controls. Preventive and therapeutic treatments with irradiated β-glucan demonstrated that the transcript level of these genes was significantly decreased which demonstrates the protective effect of β-glucan. Histological investigations revealed that diethylnitrosamine treatment affects the hepatic architecture throughout the significant severe appearance of inflammatory cell infiltration in the portal area and congestion in the portal vein in association with severe degeneration and dysplasia in hepatocytes all over hepatic parenchyma. The severity of hepatic architecture changes was significantly decreased with both β-glucan therapeutic and preventive treatments. In conclusion, irradiated β-glucan modulated signal growth factors, vascular endothelial growth factor A, extracellular signal-regulated kinase 1, and phosphatidylinositol-3-kinase, which contributed to experimental hepatocarcinogenesis. [ABSTRACT FROM AUTHOR]

Combining chemotherapy with radiotherapy potentiates the outcome of cancer treatment for the more comprehensive attack. In the current study, we continued to assess the therapeutic efficaciousness of the newly synthesized gallium nanoparticles (GaNPs) combined with low level of gamma radiation (IR), on the incidence of diethylnitrosamine (DEN)–induced hepatocellular carcinoma (HCC) in rats. Oral administration of GaNPs (1 mg/Kg b.wt.) 5 times per week for 6 weeks combined with IR to rats treated with DEN (20 mg/Kg b.wt. 5 times per week for 6 weeks) significantly reduced serum levels of alpha-fetoprotein (AFP), aspartate transferase (AST), alanine transferase (ALT), and gamma-glutamyltransferase (GGT). In addition, the immunoblotting results of matrix metalloproteinase-9 (MM-9) showed a marked downregulation of protein expression along with a significant decrease in the hepatic level of transforming growth factor β (TGF-β). Furthermore, GaNPs and/or low dose of radiation significantly elevated the level of caspase-3 gene transcript accompanied with evoked DNA fragmentation in rats treated with DEN. The ameliorative effect of GaNPs and IR well appreciated with the histopathological alteration finding in DEN groups. It can be concluded that the combination of GaNPs and/or IR can serve as a good therapeutic agent for the treatment of HCC, which ought to attract more studies. [ABSTRACT FROM AUTHOR]

Guided treatments with nanoparticles and radiotherapy are a new approach in cancer therapy. This study evaluated the beneficial antitumor effects of γ-radiation together with gallium nanoparticles against solid Ehrlich carcinoma in female mice. Gallium nanoparticles were biologically synthesized using Lactobacillus helveticus cells. Transmission electron microscopy showed gallium nanoparticles with size range of 8−20 nm. In vitro study of gallium nanoparticles on MCF-7 revealed IC50 of 8.0 μg. Gallium nanoparticles (0.1 mg/kg body weight) were injected intraperitoneally daily on the seventh day of Ehrlich carcinoma cells inoculation. Whole-body γ-radiation was carried out at a single dose of 0.25 Gy on eighth day after tumor inoculation. Biochemical analysis showed that solid Ehrlich carcinoma induced a significant increase in alanine aminotransferase activity and creatinine level in serum, calcium, and iron concentrations in liver tissue compared to normal control. Treatment of Ehrlich carcinoma–bearing mice with gallium nanoparticles and/or low dose of γ-radiation exposure significantly reduced tumor volume, decreased alanine aminotransferase and creatinine levels in serum, increased lipid peroxidation, and decreased glutathione content as well as calcium and iron concentrations in liver and tumor tissues with intense DNA fragmentation accompanied compared to untreated tumor cells. Moreover, mitochondria in the treated groups displayed a significant increase in Na+/K+-ATPase, complexes II and III with significant reduction in CYP450 gene expression, which may indicate a synergistic effect of gallium nanoparticles and/or low dose of γ-radiation combination against Ehrlich carcinoma injury, and this results were well appreciated with the histopathological findings in the tumor tissue. We conclude that combined treatment of gallium nanoparticles and low dose of gamma-radiation resulted in suppressive induction of cytotoxic effects on cancer cells. [ABSTRACT FROM AUTHOR]

Hepatitis was characterized by extreme inflammation and hepatocellular damage. Therefore, the current study aimed to gain insights into the modulation role of Cinnamic acid nanoparticles (CANPs) against acute hepatitis induced by d-Galactosamine and gamma radiation exposure (D-Gal/radiation) in the rat model and to suggest the implied molecular mechanism of CANPs. Acute hepatitis seriousness and the serum enzyme activities of ALT, AST, and ALP have been diminished upon oral administration of CANPs. Besides, the hepatic tissue levels of malondialdehyde (MDA) and nitric oxide (NO) have been significantly decreased, and the total antioxidant activity (TAO) depletion was extremely restored. Furthermore, the reduction of hepatic damage caused by pretreatment with CANPs was accompanied by significant suppression in the levels of hepatic proinflammatory cytokines (TNF-α, IL-1β, and IL-18), NF-κB, NLRP3, caspase-1 and proapoptotic protein BAX whereas anti-apoptotic protein Bcl-2 level significantly elevated as compared with D-Gal/radiation-induced acute hepatitis (AH) group. Also, CANPs suppress the D-Gal/radiation-induced IL-1β, IL-18, and ASK1 mRNA gene expression and the protein expression of TLR4 and MyD88 in the hepatic tissue. These biochemical parameters are confirmed by histological examination of the liver tissues. The present results indicated that CANPs can protect the hepatic cells from damage by both its anti-inflammatory and antioxidant influence as well as by modulating oxidation cellular pathways that have contributed to the acute severity of hepatitis. Also, CANPs is capable of suppressing apoptosis. Consequently, Nanoparticles of Cinnamic acid have the medicinal ability to protect the liver from acute hepatitis., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Acute Pancreatitis (AP) is a multifactorial disease. It was characterized by severe inflammation and acinar cell destruction. Thus, the present study was initiated to evaluate the role the of Cinnamic acid nanoparticles (CA-NPs) as a modulator for the redox signaling pathway involved in the development of pancreatitis. AP in rats was induced by L-arginine and exposure to gamma radiation. The pancreatic injury was evaluated using biochemical and histological parameters. Upon the oral administration of CA-NPs, both the severity of acute pancreatitis and the serum levels of amylase and lipase were decreased. Furthermore, the malondialdehyde (MDA) levels of the pancreatic tissue were significantly reduced and the depletion of glutathione was considerably restored. The injury and apoptosis of pancreatic tissues were markedly improved by the reduction of the caspase-3 levels. Additionally, the alleviation of pancreatic oxidative damage by CA-NPs was accompanied by a down-regulation of the NLRP3, NF-κB, and ASK1/MAPK signaling pathways. Collectively, the current findings showed that CA-NPs could protect the pancreatic acinar cell from injury not only by its antioxidant, anti-inflammatory effect but also by modulation of the redox-sensitive signal transduction pathways contributed to acute pancreatitis severity. Accordingly, cinnamic acid nanoparticles have therapeutic potential for the management of acute pancreatitis., Competing Interests: Declaration of competing interest The authors declare that they did not receive any financial support for the research., (Copyright © 2020 Elsevier B.V. All rights reserved.)

There is growing evidence that some parasitic infections can impact a variety of autoimmune diseases by disease-inducing or protecting capacities. Anti-inflammatory molecules secreted by Toxoplasma gondii and other parasites are capable of preventing some autoimmune disease like arthritis, lupus nephritis and systemic lupus erythematosus by acting on the immune system. Here we aimed to evaluate the protective efficacy of vaccination with Toxoplasma gondii (T. gondii), either gamma radiation-attenuated or not, on an adjuvant arthritis mouse model. Forty female Swiss albino mice were conducted in experiment divided into normal control; mice were injected with Complete Freund's adjuvant (CFA) into the right hind paws; mice vaccinated with irradiated T. gondii in the 3rd group and un-irradiated T. gondii in the 4th group then were injected two weeks later with CFA. Histopathological changes and IL-17, STAT6 and ROR-γ levels in the joints, as well as serum survivin and Anti-CCP, were evaluated. Also, the splenic production of TGF-β1, TGF-βR, IL-23, IL-1β, IFN-γ, TFN-∞, NF K β, MMP1 and MMP3 were assessed. Results exhibited an enhancement of the histopathological changes with diminished the rise of IL-17, STAT 6 and ROR- γ within the joints of both vaccinated groups. Also, serum survivin and Anti-CCP, as well as splenic inflammatory cytokines were reduced. It can be concluded that vaccination with un-irradiated or radiation-attenuated T. gondii exerted a protective effect against adjuvant arthritis with better pathological achievement in the radiation-attenuated vaccinated group. Using gamma radiation-attenuated parasite to exclude the delirious effects of imposing infection of live one may pave the way to new preventative modality against rheumatoid arthritis., Competing Interests: Declaration of Competing Interest The authors declare that they have no competing interest., (Copyright © 2020 Elsevier B.V. All rights reserved.)

Treatment of cancer often requires exposure to radiation, which has several limitations involving non-specific toxicity toward normal cells, reducing the efficacy of treatment. Recent studies synthesize new quinolone derivatives to satisfy other purposes such as treatment of inflammatory and malignant diseases. The main purpose of the present study is to evaluate the effect of a new quinolone derivative; 2-(1-Ethyl-4-hydroxy-2-oxo-1,2-dihydroquinolin-3-yl)-2-oxoacetic acid (EHQA) and its possible mechanism against gamma radiation (IRR) and cisplatin (Cis) induced nephrotoxicity and neurotoxicity in mice. The structure of the newly synthesized quinolone derivative was elucidated by microanalytical and spectral data, which were found consistent with the assigned structures. Exposure to Cis and IRR significantly induced renal damage manifested by a significant increase in levels of urea and creatinine. Moreover, the exposure to both Cis and IRR significantly decreased the levels of anti-apoptotic protein; Bcl-2 in both renal and brain tissue homogenate accompanied by activation of an inflammatory marker; IL-17. Immunophenoting results showed an activation of T- lymphocytes marker; CD3 and B-lymphocytes marker; CD19. Interperitonial administration of EHQA significantly ameliorated the above-mentioned parameters. Overall, the present results indicated that EHQA is a promising anti-inflammatory and anti-apoptotic agent. From the obtained results it can be concluded that EHQA could be a candidate as immunomodulatory agents. Further studies are required to establish its molecular mechanism., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Introduction: Colon Cancer remains one of the major worldwide causes of cancer related morbidity and mortality in both genders. Berberine (BBR), a major component of alkaloids that possess a variety of pharmacological properties. Objective: This study shows the ameliorating roles of berberine on 1,2 Di methyl hydrazine (DMH) induced colon cancer in male Swiss albino rats. Methods: The rats were segregated into four groups: group 1, control rats; group 2, rats were orally received berberine (75 mg/kg b.wt./day) daily for ten weeks; group 3,rats were subcutaneously injected with DMH (20 mg/kg b.wt) once a week for 8 weeks ,group 4, rats were treated firstly with berberine for two weeks before DMH intoxication and concurrently with DMH over 8 weeks. Result: DMH injection decreased the antioxidants levels (GSH and SOD) and increased inflammatory markers (MPO, MAPK and COX-2). Moreover, it downregulated apoptotic markers (Caspase-3 and P53) expression that confirmed by colon cell proliferation. The prophylactic effect of berberine was noticed as its pre-and co-administration increased antioxidants status and apoptotic markers expression that associated with inflammatory markers down-regulation with absence of proliferated colon cells. Conclusion: Therefore, the overall findings proved that the anti-proliferative effect of berberine return to its antioxidants and anti-inflammatory properties that activated the programmed cell death process., (Creative Commons Attribution License)

5, 7-Dihydroxyflavone (DHF), a natural plant flavonoid, have shown a variety of beneficial effects. Neurotoxic effects of acrylamide (ACR) or gamma irradiation (IR) have been established in humans and animals. The current study was designed to evaluate whether DHF could restrain ACR or IR induced neurotoxicity in rats and to explore the underlying mechanisms. The study was carried out by investigating some biochemical and biophysical parameters as well as histopathological examination. The daily oral administration of ACR (25mg/kg b.wt.) for 21days or exposure to single dose of IR (5Gy) induced brain damage throughout the significant decrease in catecholamine contents and brain derived neurotrophic factor (BDNF) in brain tissue with a concomitant significant decrease in serum activity of creatinine kinase-BB. Moreover, the brain levels of MDA and β-amyloid and activities of acetylcholinesterase and caspase-3 were remarkably augmented in ACR-induced rats. Additionally, the electrical properties of erythrocytes membrane were significantly disturbed. The administration of DHF (50mg/kg b.wt. daily for 21day) to rats exposed to either ACR or IR significantly reversed the alteration in all studied parameters. Histopathological investigation of brain tissues supported the neuroprotective effect of DHF on brain. From the obtained data, it can be concluded that the DHF has neuroprotective effect against ACR or IR induced-neurotoxicity., (Copyright © 2017 Elsevier B.V. All rights reserved.)

Combination therapy that targets cellular signaling pathway represents an alternative therapy for the treatment of colon cancer (CRC). The present study was therefore aimed to investigate the probable interaction of Lactobacillus rhamnosus ATCC 7469 exopolysaccharides (EPS) with low level ionizing γ radiation (γ-R) exposure against dimethylhydrazine (DMH)- induced colorectal carcinogenesis in rats. Colon cancer was induced with 20mg DMH/kg BW. Rats received daily by gastric gavage 100mg EPS/Kg BW concomitant with 1Gy γ-R over two months. Colonic oxidative and inflammatory stresses were assessed. The change in the expression of p-p38 MAPK, p-STAT3, β-catenin, NF-kB, COX-2 and iNOS was evaluated by western blotting and q-PCR. It was found that DMH treatment significantly induced colon oxidative injury accompanied by inflammatory disturbance along with increased protein expression of the targeted signaling factors p-p38 MAPK, p-STAT3 and β-catenin. The mRNA gene expression of NF-kB, COX-2 and iNOS was significantly higher in DMH-treated animals. It's worthy to note that colon tissues with DMH treatment showed significant dysplasia and anaplasia of the glandular mucosal lining epithelium with loses of goblet cells formation, pleomorphism in the cells and hyperchromachia in nuclei. Interestingly, EPS treatment with γ-R exposure showed statistically significant amelioration of the oxidative and inflammatory biomarkers with modulated signaling molecular factors accompanied by improved histological structure against DMH-induced CRC. In conclusion, our findings showed that Lactobacillus rhamnosus ATCC 7469 EPS with low level γ-R in synergistic interaction are efficacious control against CRC progression throughout the modulation of key signaling growth factors associated with inflammation via antioxidant mediated anti-inflammatory and anti-proliferative activities., (Copyright © 2017 Elsevier Masson SAS. All rights reserved.)

Hepatic encephalopathy (HE) is a syndrome resulting from acute or chronic liver failure. This study was designed to evaluate the effect of rutin on thioacetamide (TAA) or γ-radiation-induced HE model. Animals were received with TAA (200mg/kg, i.p.) twice weekly for four weeks or exposed to 6Gy of γ-radiation to induce HE then groups orally treated with rutin (50mg/kg b.wt.) for four weeks. At the end of experiment, blood, liver and brain samples were collected to assess biochemical and biophysical markers as well histopathological investigations. TAA or γ-radiation exposed rats experienced increases in serum activities of ALT, AST, ALP and ammonia level. Also an alteration in relative permeability and conductivity of erythrocytes was observed. Furthermore, cytokines levels and AChE activity were induced whereas the activities of HO-1 and neurotransmitters contents were depleted. TAA or γ-radiation caused distortion of hepatic and brain architecture as shown by histopathological examination. Treatment with rutin resulted in improvement in liver function by the decline in serum AST and ALT activities and reduction in serum ammonia level. In addition, the administration of rutin significantly modulated the alteration in cytokines levels and neurotransmitters content. Histopathological examinations of liver and brain tissues showed that administration of rutin has attenuate TAA or radiation-induced damage and improve tissue architecture. Consequently, rutin has been a powerful hepatoprotective effect to combat hepatic encephalopathy associated hyperammonemia and its consequential damage in liver and brain., (Copyright © 2017 Elsevier B.V. All rights reserved.)

This study investigated the possible beneficial effects of grape seed oil (GSO) on carbon tetrachloride (CCl4)-induced acute neurotoxicity in γ-irradiated rats. A statistical significant decrease in superoxide-dismutase (SOD), catalase (CAT), and glutathione-peroxidase (GPx) activities and reduced glutathione (GSH) content were exhibited. Further, a significant elevation in malondialdehyde (MDA), nitric oxide (NO), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and transforming growth factor-beta-1 (TGF-β1) levels was observed. Furthermore, xanthine oxidase (XO) and inducible nitric oxide synthase (iNOS) gene expression were elevated in the γ-irradiated animals treated with an acute dose of CCl4. The pretreatment of GSO exerts significant amelioration of the studied parameters. In conclusion, this study demonstrated that GSO has a neuroprotective effect against CCl4-induced brain injury in γ-irradiated rats, which is likely attributed to its ability to scavenge the free radicals, suppress the inflammatory responses, improve the activity of the antioxidant enzymes and inhibit the XO and iNOS gene expression levels., (Copyright © 2015 Elsevier B.V. All rights reserved.)