Inflammatory mediators-induced DNA damage in liver and brain injury: Therapeutic approach of 5-Methoy-N-acetyltryptamine.

The pathophysiology of hepatic and cerebral damage includes various molecular and signalling pathways. Assessment of inflammation-induced DNA damage is one of the principal issues for investigating organ distortion and mutation. The current study was premeditated to discover the prophylactic role of 5-Methoy-N-acetyltryptamine (5-MNAT) and/or Quercetin (QR) versus sodium nitrite (NaNO) induced liver and brain injury in a rat model, as well as to clarify the different cross-linked inflammatory pathways and neurotransmitters.

Fischer's oligopeptide ratio in ischemic hypoxia: prophylactic amendment of sophoretin and melatonin supplementation.

The fundamental pathophysiology of ischemic-hypoxia is oxygen depletion. Fischer's ratio is essential for monitoring hypoxia intensity. the current study highlighted the prophylactic role of sophoretin (QRC) and/or melatonin (MLN) versus sodium nitrite (SN) brain hypoxia.

Impact of HIF1-α/TGF-β/Smad-2/Bax/Bcl2 pathways on cobalt chloride-induced cardiac and hepatorenal dysfunction.

Background: Cobalt chloride (CoCl) is a ferromagnetic ubiquitous trace element extensively dispersed in the environment. Nevertheless, it may merit human hazard.

Aim: Excess cobalt can harm vital organs this paves the way to elucidate the toxic impact of CoCl on the liver, kidney and heart.

Special Issue "Computer Aided Diagnosis Sensors".

Sensors used to diagnose, monitor or treat diseases in the medical domain are known as medical sensors [...

Sengers syndrome: a rare case of cardiomyopathy combined with congenital cataracts in an infant: post-mortem case report.

Sengers syndrome is a rare autosomal recessive disorder caused by a mutation in the Acylglycerol Kinase (AGK) gene with subsequent mitochondrial dysfunction. It is a combination of cardiomyopathy, skeletal myopathy, congenital bilateral cataracts, and lactic acidosis following exertion. The current study describes an extremely rare case of Sengers syndrome that is diagnosed during post-mortem examination.

Inhibition of NF-κB and the oxidative stress -dependent caspase-3 apoptotic pathway by betaine supplementation attenuates hepatic injury mediated by cisplatin in rats.

Background: Cisplatin is a major anti-cancer drug commonly used in the treatment of various cancers; nevertheless, the associated hepatotoxicity has limited its clinical application. The aim of this investigation is to test the impact of betaine supplementation on cisplatin-induced hepatotoxicity.

Methods: Animals were allocated into four groups; normal control group (control betaine group (250 mg/kg/day, po for twenty six days), cisplatin group (single injection of 7 mg/kg, ip) and betaine + cisplatin group (received betaine for twenty one days before cisplatin injection and daily after cisplatin for five days).

Study of relationship between total vitamin D level and NAFLD in a sample of Egyptian patients with and without T2DM.

Background: Non-alcoholic fatty liver disease (NAFLD) is increasing recently due to increasing the prevalence of obesity. Insulin resistance (IR) is the mutual pathological cause for both T2DM and NAFLD. Vitamin D acts against IR by its anti-inflammatory and regulation of insulin secretion as pancreatic beta cells express vitamin D receptor (VDR).

Roles of some antioxidants in modulation of cardiac myopathy induced by sodium nitrite via down-regulation of mRNA expression of NF-κB, Bax, and flt-1 and suppressing DNA damage.

Unlabelled: The underlying pathology of cardiac damage involves various molecular and signaling pathways. Therefore, this study aimed to explore the role of Quercetin (Querc), alone or in combination with Melatonin (Melat) against cardiac damage induced by sodium nitrite (Sod nit), as well as to elucidate different signaling pathways. Querc and Melat were injected intraperitoneally (i.

Mitigative role of garlic and vitamin E against cytotoxic, genotoxic, and apoptotic effects of lead acetate and mercury chloride on WI-38 cells.

Background: Lead acetate (Led) and mercury chloride (Mer) represent important ecological and public health concerns due to their hazardous toxicities. Naturally found products play a vital role in chemopreventive agent innovation. The current study aimed to assess the modifying effect of garlic (Gar) and/or vitamin E (Vit E) against the half-maximal inhibitory concentration (IC50) Led and/or Mer-induced cytotoxic, genotoxic and apoptotic effects.

Downregulation of and Gene Expression by Some Antioxidants in Rats Under Sodium Nitrite-Induced Hypoxic Stress.

This study assessed the effect of L-arginine (L-argin), carnosine (carno), or their combination in the amelioration of certain biochemical indices induced in the liver of hypoxic rats. Hypoxia was induced via sodium nitrite (S.nit) injection at a dose of 75 mg/kg.

Prophylactic administration of carnosine and melatonin abates the incidence of renal toxicity induced by an over dose of titanium dioxide nanoparticles.

The alleviative effects of two antioxidants, carnosine (Car) and melatonin (Mel), against titanium dioxide nanoparticles (TiO -NPs) toxicity-induced oxidative and inflammatory renal damage were examined in rats. Administration of these antioxidants along with TiO -NPs effectively reduced serum urea, uric acid, creatinine, glucose, tumor necrosis factor-α, interleukin-6, C-reactive protein, immunoglobulin G, vascular endothelial growth factor, and nitric oxide, as well as a significant amelioration of the decrease in glutathione levels in renal tissue was observed, compared to those in rats treated with TiO -NPs alone. The renoprotective properties of the antioxidants were confirmed by reduced intensity of renal damage as demonstrated by histological findings.

Attenuation of DNA damage and mRNA gene expression in hypoxic rats using natural antioxidants.

This study aimed to explore the efficiency of carnosine (Cs) and/or l-arginine (Agn) in the downregulation of apoptotic and inflammatory molecule expression and DNA damage caused hepatic injury in response to sodium nitrite (Sd)-induced hypoxia in rats. Rats were injected with Sd; Agn or/and Cs were administrated prior to Sd intoxication. Sd significantly decreased hemoglobin concentration and Bcl-2 mRNA expression, while increased expressions of apoptotic markers (Bax and caspase), tumor necrosis factor-α, nuclear factor kappa B, and C-reactive protein and the oxidative DNA damage in hepatic tissue.

Downregulation of HIF1-α, Smad-2, AKT, and Bax gene expression in sodium nitrite-induced lung injury via some antioxidants.

The aim of the current study is to evaluate the efficacy of pretreatment with either l-arginine (L-arg) or Carnosine (Car) and their combination in ameliorating some of the biochemical indices induced in the lung of sodium nitrite (NaNO )-intoxicated rats. The results revealed that NaNO significantly increased serum tumor necrosis factor-α, C-reactive protein, heat shock proteins-70, vascular endothelial growth factor, and Interleukin 6. Moreover, transforming growth factor-β, hypoxia-inducible factor, Smad-2, Protein Kinase B (AKT), and Bax were overexpressed, whereas Bcl2 protein was downregulated compared with the normoxic group.

Role of Different Natural Antioxidants in the Modulation of mRNA-expression of Apoptotic Molecules in the Livers of Carbon Tetrachloride-Intoxicated Rats.

Overexpression of nuclear factor (NF-κB) or activation of Smad3 by transforming growth factor β (TGF-β1) induced by oncogenes results in overexpression of fibrotic processes and hence cell death. The objective of this study is to examine whether Silymarin (Sil) alone or in combination with Vitamin E (Vit E) and/or Curcumin (Cur) plays a modulatory role against the overexpression of NF-κB, and TGF-β that induced in response to carbon tetrachloride (CCl) administration. The present work revealed that CCl induced elevation of in serum alanine aminotransferase (ALT), Apoptosis regulator (Bax), Smad3, TGF-β, and NF-kB hepatic mRNA expression (using Real-time PCR), administration of Sil alone downregulated these expressions.

Quercetin inhibits sodium nitrite-induced inflammation and apoptosis in different rats organs by suppressing Bax, HIF1-α, TGF-β, Smad-2, and AKT pathways.

The objective of this work is to study the protective effects of Quercetin against sodium nitrite-induced hypoxia on liver, lung, kidney and cardiac tissues, also to explore novel mechanism of this compound. Male albino rats were injected with sodium nitrite (75 mg/kg). Quercetin (200 mg kg ,- i.

New mechanism in the modulation of carbon tetrachloride hepatotoxicity in rats using different natural antioxidants.

Transforming growth factor-β (TGF-β1) enhances the expression of apoptosis induced by certain cytokines and oncogenes. Activation of small mother against decapentaplegic (Smads) by TGF-β results in fibrotic, apoptotic processes. PI-3/AKT focal adhesion kinase-phosphatidylinositol3-kinase (AKT), the mitogen-activated protein kinase (MAPK) and signal transducer and activator of transcription-3 (STAT3) pathways are influence in COX-2 and VEGF-stimulating pathways.