NADPH oxidase 2 does not contribute to early reperfusion-associated reactive oxygen species generation following transient focal cerebral ischemia

Excess production of reactive oxygen species （ROS） critically contributes to occurrence of reperfusion injury, the paradoxical response of ischemic brain tissue to restoration of cerebral blood flow. However, the enzymatic sources of ROS generation remain to be unclear. This study examined Nox2-ontaining NADPH oxidase （Nox2） expression and its activity in ischemic brain tissue following post-ischemic reperfusion to clarify the mechanism of enzymatic reaction of ROS. Male Sprague-Dawley rats were subjected to 90-minute middle cerebral artery occlusion, followed by 3 or 22.5 hours of reperfusion. Quantitative reverse transcriptase PCR and western blot assay were performed to measure mRNA and protein expression of Nox2. Lucigenin fluorescence assays were performed to assess Nox activity. Our data showed that Nox2 mRNA and protein expression levels were significantly increased （3.7-fold for mRNA and 3.6-fold for protein） in ischemic brain tissue at 22.5 hours but not at 3 hours following post-ischemic reperfusion. Similar results were obtained for the changes of NADPH oxidase activity in ischemic cerebral tissue at the two reperfusion time points. Our results suggest that Nox2 may not contribute to the early burst of reperfusion-related ROS generation, but is rather an important source of ROS generation during prolonged reperfusion.

Concurrent severe hepatotoxicity and agranulocytosis induced by Polygonum multiflorum:A case report

BACKGROUND Various types of drug-induced liver injury are induced by Polygonum multiflorum(PM);however,it rarely causes neutropenia.Herein,we report the case of a 65-year-old woman with concurrent severe hepatotoxicity and agranulocytosis induced by PM.CASE SUMMARY A 65-year-old woman reported with severe hepatotoxicity and agranulocytosis 17 d after ingestion of PM.The results of the Roussel Uclaf Causality Assessment Method demonstrated a highly probable relationship between hepatotoxicity and PM,with a total score of 10.The Naranjo algorithm results indicated that agranulocytosis had a probable relationship with PM,with an overall score of 6.Granulocyte colony-stimulating factor(for once),a steroid,compound glycyrrhizin,and polyene phosphatidylcholine therapy were initiated.After 15 d of treatment,there was a gradual improvement in liver biochemistry,leukocytes,and neutrophils levels.CONCLUSION Concurrent hepatotoxicity and agranulocytosis are rare and critical adverse drug reactions of PM,which should be highly valued.

Lychee seed saponins improve cognitive function and ameliorate hippocampal neuronal injury in Alzheimer disease rat model induced by Aβ_(25-35) through AKT/GSK3β pathway

OBJECTIVE Lychee seed,a famous traditional Chinese medicine,recently were reported to improve the learning and memory abilities in mice.However,it is still unclear whether lychee seed saponins(LSS)can improve the cognitive function and associated mechanisms.METHODS In present studies,we established the Alzheimer disease(AD)model by injecting Aβ25-35 into the lateral ventricle of rats.Then the spatial learning and memory abilities of LSS-treated rats were evaluated with the Morris water maze,meanwhile the protein expressions of AKT,GSK3β and Tau in the hippocampal neuron were analyzed by immunohistochemistry and Western blotting.RESULTS The results showed LSS can improve the cognitive functions of AD rats through shortening the escape latency,increasing the number across the platform,platform quadrant dwell time and the percentage of the total distance run platform quadrant.The protein expression of AKT was significantly up-regulated and that of GSK3β and Tau were decreased remarkably in the hippocampal CA1 area.CONCLUSION Our study is the first to show that LSS significantly improve the cognitive function and prevent hippocampal neuronal injury of the rats with AD by activation of the PI3K/AKT/GSK3βsignaling pathway,suggesting LSS may be developed into the nutrient supplement for the treatment of AD.

Targeting autophagy as a therapeutic strategy for identification of liganans from Peristrophe japonica in Parkinson’s disease

Dear Editor,PD is characterized by the loss of dopaminergic neurons in substantia nigra,and the loss of dopamine resulting in motor deficit.1 Its main pathological hallmarks include the genetic mutations of gene such as a-synudein.2 Increasing study showed that the dopaminergic neurons in midbrain are sensitive and damaged by the PD toxins.