Objective:To observe any effect of an enriched environment (EET) on cognitive functioning and sonic hedgehog (SHH) signaling in rats modeling cerebral ischemia.Methods:Sixty adult male Sprague-Dawley rats were randomly divided into a blank control group, a model group and a training group. A model of cerebral ischemia was established in the model and training groups by thread thrombus. The training group was given an EET. After 7 and 14 days, the rats′ cognition was tested using the Morris water maze and the platform jumping test. Apoptosis of brain cells in the hippocampus was detected by using TUNEL staining, and the expression of SHH, Gli2 and PTCH1 proteins in the hippocampus were measured using qRT-PCRs, western blotting and immunohistochemistry.Results:After 14 days the average escape latency in the Morris water maze test had shortened more in the training group than in the model group, while the average swimming speed, the number of platform crossings and the time spent in the quadrant had increased significantly more. They also received fewer electric shocks and spent significantly less time on the platform in the platform jumping test on average. Apoptosis in the hippocampus after 14 days was significantly less in the training group with significantly greater expression of SHH and Gli2 protein and significantly less PTCH1 protein expression.Conclusion:An EET can significantly improve cognition after cerebral ischemia, at least in rats. Its mechanism may be related to enhanced activation of the SHH signaling pathway.

Linezolid is an oxazolidinone antibacterial agent used in infections caused by gram-positive cocci such as methicillin-resistant staphylococcus aureus, penicillin-resistant pneumococcus and vancomycin-resistant enterococcus. Lactic acidosis is one of the adverse reactions of linezolid. The risk factors of lactic acidosis caused by linezolid are long-term exposure, liver dysfunction, renal dysfunction, mitochondrial DNA A2706G polymorphism, combined use of drugs affecting mitochondrial function, etc. The symptoms of lactic acidosis caused by linezolid are nausea, vomiting, drowsiness, shortness of breath, tachycardia, and hypotension, etc., which can be identified early by close monitoring of laboratory indicators such as blood lactic acid, pH, and blood drug concentration. The mechanism of lactic acidosis induced by linezolid may be related to mitochondrial toxicity. The lactic acidosis of linezolid can be caused by reducing drug dose, stopping drug or even in vitro renal replacement therapy, and strengthening symptomatic support therapy if necessary. This review is intended to provide ideas for the clinical prevention and treatment of lactate acidosis caused by linezolid.