Therapeutic Effect of Levetiracetam Against Thioacetamide-Induced Hepatic Encephalopathy Through Inhibition of Oxidative Stress and Downregulation of NF-κB, NLRP3, iNOS/NO, Pro-Inflammatory Cytokines and Apoptosis.

Hepatic encephalopathy (HE) is a serious brain disorder which associated with neurological and psychiatric manifestations. Oxidative stress and neuroinflammation and apoptosis play main roles in the development of brain damage in HE. Levetiracetam is an antiseizure drug with established antioxidant and anti-inflammatory activities.

Carvedilol attenuates inflammatory reactions of lipopolysaccharide-stimulated BV2 cells and modulates M1/M2 polarization of microglia via regulating NLRP3, Notch, and PPAR-γ signaling pathways.

Microglial cells coordinate immune responses in the central nervous system. Carvedilol (CVL) is a non-selective β-blocker with anti-inflammatory and anti-oxidant effects. This study aims to investigate the anti-inflammatory effects and the underlying mechanisms of CVL on lipopolysaccharide (LPS)-induced inflammation in microglial BV2 cells.

Levetiracetam attenuates experimental ulcerative colitis through promoting Nrf2/HO-1 antioxidant and inhibiting NF-κB, proinflammatory cytokines and iNOS/NO pathways.

Ulcerative colitis (UC) is a serious inflammatory disease of the colon. The pathogenic mechanisms of UC involve the activation of inflammatory and oxidative stress responses in the colon. Levetiracetam is an antiepileptic drug with anti-inflammatory and antioxidant effects.

Carvedilol attenuates brain damage in mice with hepatic encephalopathy.

Brain injury is the most common and serious consequence of hepatic encephalopathy (HE), and its pathophysiology is poorly understood. Excessive inflammatory, oxidative and apoptotic responses are the major mechanisms involved in the progression of brain injury induced by HE. Carvedilol is an adrenergic receptor antagonist with pronouncedantioxidant and anti-inflammatory activity.

Carvedilol attenuates acrylamide-induced brain damage through inhibition of oxidative, inflammatory, and apoptotic mediators.

Objectives: Acrylamide is a potent neurotoxic compound and has harmful effects on brain cells. Acrylamide promotes oxidative, inflammatory, and apoptotic mediators in the CNS leading to neurological disorders. The goal of the current study was to examine the potential protective effect of carvedilol and its underlying mechanisms in a mouse model of acrylamide-induced brain injury.

Taxonomical Investigation, Chemical Composition, Traditional Use in Medicine, and Pharmacological Activities of Flueck.

Aromatic oleo-gum-resin secreted from , reputed as frankincense, is widely used in traditional medicine to treat Alzheimer's disease, gastric disorders, hepatic disorders, etc. Frankincense is also used in the cosmetic, perfume, and beverage and food industries. Frankincense is a rich resource for bioactive compounds, especially boswellic acids and derivatives.

Methylsulfonylmethane protects against ethanol-induced brain injury in mice through the inhibition of oxidative stress, proinflammatory mediators and apoptotic cell death.

Excessive ethanol consumption causes brain injury through oxidative stress, inflammation and apoptotic cell death. Methylsulfonylmethane (MSM) is a natural compound that has therapeutic effects on oxidative and inflammatory disorders. The aim of this study was to investigate the protective effect and underlying mechanisms of MSM on ethanol-induced brain injury in an experimental model.

Acrylamide exposure aggravates the development of ulcerative colitis in mice through activation of NF-κB, inflammatory cytokines, iNOS, and oxidative stress.

Objectives: Acrylamide is a toxic compound that forms during food processing at high temperatures. Acrylamide has been shown to induce toxicity in various organs in the body. This study aimed to investigate the effect of acrylamide exposure on the susceptibility of the colon to ulcerative colitis in a mouse model.

Thalidomide reduces glycerol-induced acute kidney injury by inhibition of NF-κB, NLRP3 inflammasome, COX-2 and inflammatory cytokines.

Acute kidney injury (AKI) is an important clinical complication of rhabdomyolysis. The inflammatory processes are involved in the pathogenesis of AKI induced by rhabdomyolysis. Thalidomide is an anti-inflammatory agent that has been used in the treatment of inflammatory disorders.

Carvedilol prevents pancreatic β-cell damage and the development of type 1 diabetes in mice by the inhibition of proinflammatory cytokines, NF-κB, COX-2, iNOS and oxidative stress.

Inflammation is one of the main mechanisms of pancreatic β-cell damage and the development of type 1 diabetes (T1D). Carvedilol, a beta-adrenergic receptor blocker, has been demonstrated to have anti-inflammatory and antioxidant effects. The aim of this study was to investigate the protective effect of carvedilol against pancreatic β-cell damage and the development of T1D in an experimental model.

The Neuroprotective Effect of Mesna on Cisplatin-Induced Neurotoxicity: Behavioral, Electrophysiological, and Molecular Studies.

Peripheral neuropathy and cognitive impairments following cisplatin administration may interfere with the clinical usage of the drug. Mesna is a chemoprotective agent with anti-inflammatory and anti-oxidant effects. Our study aimed to investigate the protective effects of mesna against cisplatin-induced neurotoxicity.

RIPK3-MLKL-Mediated Neutrophil Death Requires Concurrent Activation of Fibroblast Activation Protein-α.

Cytokine-primed neutrophils can undergo a nonapoptotic type of cell death using components of the necroptotic pathway, including receptor-interacting protein kinase-3 (RIPK3), mixed lineage kinase-like (MLKL) and NADPH oxidase. In this report, we provide evidence for a potential role of serine proteases in CD44-mediated necroptotic death of GM-CSF-primed human neutrophils. Specifically, we observed that several inhibitors known to block the enzymatic function of fibroblast activation protein-α (FAP-α) were able to block CD44-mediated reactive oxygen species production and cell death, but not FAS receptor-mediated apoptosis.

Febuxostat attenuates ulcerative colitis by the inhibition of NF-κB, proinflammatory cytokines, and oxidative stress in mice.

Ulcerative colitis is a chronic inflammatory disorder characterized by oxidative stress and upregulation of proinflammatory mediators in colonic tissue. Febuxostat, a xanthine oxidase inhibitor has been shown to exert anti-inflammatory and antioxidant effects. The aim of this study was to investigate the protective effect of febuxostat against ulcerative colitis, and to elucidate the potential mechanisms involved.

Methylsulfonylmethane is effective against gastric mucosal injury.

Methylsulfonylmethane (MSM) is a natural organosulfur compound has been widely used as a dietary supplement. MSM has protective effects against various disorders through its anti-inflammatory and antioxidant properties however the effect of MSM on gastric mucosal injury remains unclear. The aim of the present study is to determine whether MSM has beneficial effects on ethanol/HCl-induced gastric ulcer in mice.

Carvedilol attenuates paraquat-induced lung injury by inhibition of proinflammatory cytokines, chemokine MCP-1, NF-κB activation and oxidative stress mediators.

Paraquat is a highly toxic herbicide that selectively accumulates in the lungs and causes pulmonary damage through the oxidative and inflammatory processes. Carvedilol is a nonselective beta and alpha-adrenergic blocking agent that has been shown to possess powerful antioxidant and anti-inflammatory properties. In the present study, we evaluated the protective effects and the underlying mechanisms of carvedilol on paraquat-induced lung injury in a mouse model.

Gastroprotective effect of 2-mercaptoethane sulfonate against acute gastric mucosal damage induced by ethanol.

Gastric mucosal damage induced by ethanol is a serious medical problem. Recent evidences suggest that reactive oxygen species and inflammatory mediators play a key role in the destruction of gastric mucosa. The present study was aimed to evaluate the potential beneficial effect of MESNA (2-mercaptoethane sulfonate) against ethanol-induced gastric mucosal damage in mice.

The effect of thalidomide on ethanol-induced gastric mucosal damage in mice: involvement of inflammatory cytokines and nitric oxide.

Excessive ethanol ingestion causes gastric mucosal damage through the inflammatory and oxidative processes. The present study was aimed to evaluate the protective effect of thalidomide on ethanol-induced gastric mucosal damage in mice. The animals were pretreated with vehicle or thalidomide (30 or 60 mg/kg, orally), and one hour later, the gastric mucosal injury was induced by oral administration of acidified ethanol.

Thalidomide ameliorates cisplatin-induced nephrotoxicity by inhibiting renal inflammation in an experimental model.

Cisplatin is a platinum-based chemotherapy drug. However, its chemotherapeutic use is restricted by serious side effects, especially nephrotoxicity. Inflammatory mechanisms have a significant role in the pathogenesis of cisplatin-induced nephrotoxicity.

Effect of Methylsulfonylmethane Pretreatment on Aceta-minophen Induced Hepatotoxicity in Rats.

Objective(s): Methylsulfonylmethane (MSM) is a sulfur-containing compound found in a wide range of human foods including fruits, vegetables, grains and beverages. In this study the effect of MSM pretreatment on acetaminophen induced liver damage was investigated.

Materials And Methods: Male Sprague Dawley rats were pretreated with 100 mg/kg MSM for one week.

Anti-inflammatory effect of thalidomide in paraquat-induced pulmonary injury in mice.

Thalidomide has been used in inflammatory and autoimmune disorders due to its anti-inflammatory activity. Paraquat (PQ) poisoning causes severe lung injury. PQ-induced pulmonary inflammation and fibrosis are due to its ability to induce oxidative stress, inflammatory and fibrotic reactions.

Effect of methylsulfonylmethane on paraquat-induced acute lung and liver injury in mice.

Methylsulfonylmethane (MSM) is a natural organosulfur compound that exhibits antioxidative and anti-inflammatory effects. This study was carried out to investigate the effect of MSM on paraquat (PQ)-induced acute lung and liver injury in mice. A single dose of PQ (50 mg/kg, i.

Effect of captopril on TNF-α and IL-10 in the livers of bile duct ligated rats.

Background: The renin-angiotensin system has an important role in hepatic inflammation and fibrosis. Renin-angiotensin system blockade by angiotensin-converting enzyme (ACE) inhibitors provides some protective effects against hepatic fibrogenesis. Captopril as an ACE inhibitor can decrease inflammatory mediators and attenuate hepatic fibrosis in the livers of bile duct ligated (BDL) rats.