Cerebral ischemia/reperfusion causes complex pathological mechanisms that lead to brain tissue damage. Usnic acid is a lichen secondary metabolite that has many different biological properties including anti-inflammatory and anti-oxidant activities. Therefore, the objective of the current study was to investigate the neuroprotective effects of usnic acid on apoptotic cell death, neuroinflammation, anti-oxidant enzyme activities, and oxidative stress levels after transient cerebral ischemia/reperfusion. Forty-two male Wistar rats were randomly assigned to three groups (sham, ischemia/reperfusion, and ischemia/reperfusion+usnic acid). Ischemia was induced by 20 min occlusion of common carotid arteries. Injection of usnic acid (25 mg/kg, intraperitoneally) and saline was done at the beginning of reperfusion time. Morris water maze was applied to assess spatial memory. The protein expression amount was measured using immunohistochemical and immunofluorescence staining. Spectrophotometric assay was performed to determine the levels of anti-oxidant enzymes. Usnic acid significantly reduced caspase-3, glial fibrillary acidic protein- positive and ionized calcium-binding adaptor molecule 1-positive cells ( 0.001) and enhanced spatial memory disorders ( 0.05) due to brain ischemia. In addition, treatment with usnic acid improves effects in the antioxidant system following cerebral ischemia ( 0.05). Our findings indicate that usnic acid has neuroprotective properties, which possibly is applicable as a promising candidate for cerebral injuries caused by ischemia. Our findings indicate that usnic acid has neuroprotective properties, which possibly is applicable as a promising candidate for cerebral injuries caused by ischemia. Effects of ethyl acetate extract of (EES) on brain-gut peptides and interstitial cells of gastric Cajal in rats with diabetic gastroparesis were explored. Rats were divided into six groups normal control group (NC), diabetic gastroparesis model group (DGP), low, medium, and high dose of EES groups (LES, MES, and HES, respectively), and metoclopramide positive group (MPG). DGP rats were induced by streptozotocin (STZ) combined with a high-sugar-high-fat diet. The gastric emptying was measured by the phenol red labeling method. Enzyme-linked immunosorbent assay (ELISA) was employed to determine the concentrations of serum ghrelin, gastrin (GAS), somatostatin (SS), and vasoactive intestinal peptide (VIP). The expressions of c-Kit and its natural ligand stem cell factor (SCF) in gastric tissues were determined by Western blot and immunofluorescence. Gastric emptying rate increased in a different degree after intervention by EES, among which MES and HES groups showed a significant effect (compared with DGP, <0.01) and the HES group was equivalent to the MPG group; serum ghrelin and content of serum GAS increased while SS and VIP decreased (compared with the DGP group, <0.05 or <0.01); c-Kit and SCF protein expressions in gastric tissue increased (compared with DGP group, <0.05 or <0.01). EES significantly improved gastric emptying by regulating gastrointestinal hormone excretion and c-Kit/SCF signaling pathway. Our study provides a pharmacological basis for the use of the EES in the treatment of DGP. https://www.selleckchem.com/Wnt.html However, the detailed molecular mechanism remains to be clarified. EES significantly improved gastric emptying by regulating gastrointestinal hormone excretion and c-Kit/SCF signaling pathway. Our study provides a pharmacological basis for the use of the EES in the treatment of DGP. However, the detailed molecular mechanism remains to be clarified. The effects of low dose amphetamine on oxidative stress and rotenone-induced neurotoxicity and liver injury were examined in a mice model of Parkinson's disease. Male mice were treated with rotenone (1.5 mg/kg, every other day for two weeks, subcutaneously). Mice received either the vehicle or amphetamine intraperitoneally at doses of 0.5, 1.0, or 2.0 mg/kg. Oxidative stress was assessed by measurement of the lipid peroxidation product malondialdehyde (MDA), nitric oxide (NO), total anti-oxidant capacity (TAC), and paraoxonase-1 (PON-1) activity in the brain and liver. In addition, brain concentrations of nuclear factor kappa B (NF-κB) and tyrosine hydroxylase were determined and histopathology and Bax/Bcl-2 immunohistochemistry were performed. The levels of lipid peroxidation and NO were increased and TAC and PON-1 were decreased significantly compared with vehicle-injected control mice. There were also significantly increased NF-κB and decreased tyrosine hydroxylase in the brain following rotenone administration. These changes were significantly attenuated by amphetamine. Rotenone caused neurodegenerative changes in the substantia nigra, cerebral cortex, and hippocampus. The liver showed degenerative changes in hepatocytes and infiltration of Kupffer cells. Bax/Bcl2 ratio was significantly increased in brain and liver tissues. Amphetamine prevented these histopathological changes and the increase in apoptosis evoked by rotenone. These results suggest that low dose amphetamine exerts anti-oxidant and anti-apoptotic effects, protects against rotenone-induced neurodegeneration, and could prevent neuronal cell degeneration in Parkinson's disease. These results suggest that low dose amphetamine exerts anti-oxidant and anti-apoptotic effects, protects against rotenone-induced neurodegeneration, and could prevent neuronal cell degeneration in Parkinson's disease. Despite effective anticancer effects, the use of doxorubicin (DOX) is hindered due to its cardio and neurotoxicity. The neuroprotective effect of adrenomedullin (AM) was shown in several studies. The present study aimed to evaluate the possible protective effects of AM against DOX-induced toxicity in dorsal root ganglia (DRGs) neurons. Rat embryonic DRG neurons were isolated and cultured. The effect of various concentrations of DOX (0.0 to 100 µM) in the absence or presence of AM (3.125 -100 nM) on cell death, apoptosis, oxidative stress, expression of tumor necrosis-α (TNF-α), interleukin1- β (IL-1β), inducible nitric oxide synthase (iNOS), matrix metalloproteinase (MMP) 3 and 13, and SRY-related protein 9 (SOX9) were examined. Based on MTT assay data, DOX decreased the viability of DRG neurons in a dose and time-dependent manner (IC =6.88 µm) while dose-dependently, AM protected DRG neurons against DOX-induced cell death. Furthermore, results of annexin V apoptosis assay revealed the protective effects of AM (25 nm) against DOX (6.