ABSTRACT
@#【Objective】 As the main active ingredient of Tibetan medicine Hongjingtian (Rhodiolae Crenulatae Radix et Rhizoma), salidroside (Sal) has a good anti-apoptotic potential. Currently, there are some conflicting results on the anti-apoptotic mechanisms of Sal. Here we conducted a systematic review and meta-analysis to provide the preclinical evidence of its anti-apoptotic properties in preventing and treating hypoxic-ischemic cerebral damage(HICD). 【Methods】 The literature on the anti-apoptotic potential of Sal in the treatment of HICD from January 1, 1980 to November 9, 2021 was searched online using Chinese databases including Chinese National Knowledge Infrastructure (CNKI), China Science and Technology Journal Database (VIP), and Wanfang Database, and English databases including PubMed and Web of Science. The quality of the included articles was evaluated by the Cochrane Collaboration network bias risk assessment criteria, and meta-analysis was performed using RevMan 5.3 software. 【Results】 A total of 40 articles were finally included. Among the 40 articles, 30 were about in vivo animal experiments and 17 about in vitro cell experiments, and 7 of them included both animal and cell experiments. After analysis, it was found that Sal had significant effects on disease-related indicators of HICD (P < 0.05), such as cerebral infarctsize and brain water content. As to in vivo studies, Sal mainly affects the expressions of apoptotic factors through antiinflammation, anti-oxidation, activation of complement pathway, and regulation of signal transduction and autophagy, thus exerting anti-apoptotic potential in treating HICD. While for in vitro studies, Sal plays the anti-apoptotic role in HICD models mainly through anti-oxidation, anti-inflammation, reduction of Ca2+ overload, regulation of mitochondrial function, signal transduction, and C3 complement. 【Conclusion】 Sal can take anti-apoptotic effects to prevent and treat HICD through mechanisms such as anti-inflammation, anti-oxidation, enhanced autophagy, complement and signal transduction, regulation of mitochondrial membrane potential, and reduction of Ca2 + overload.
ABSTRACT
Objective To investigate the effect of the cerebral protection and possible mechanism of fasudil for hypoxic-ischemic cerebral damage (HIBD) in neonatal rats. Methods The HBID model was established, then the mice were randomly divided into different groups. The expressions ofα-SMA and ROCK-2 were detected in the newborn rats with ischemia. Results Compared with the model group, expressions of α-SMA, ROCK-2 decreased in each treatment group with significant differences (P < 0.05 or P < 0.01). Following with the increases of administration dose and the administration time, expressions of α-SMA, ROCK-2 decreased gradually with significant differences (P<0.05 or P<0.01). Conclusion Fasudil can reduce the expressions of α-SMA, ROCK-2 in the newborn mice with hypoxic-ischemic brain damage to attenuate the brain tissue hypoxic-ischemic injury. The protective effect on brain is significant by giving high-dose fasudil in the early neonatal rat HIBD (0 h).
ABSTRACT
Objective To study the relationships between the serum neuron specific enolase(NSE) and the severity and prognosis of brain damage in critically ill children. Methods A total of 96 critically ill children with acute brain injury admitted in our hospital Pediatric Intensive Care Unit (PICU) from January to June 2013 were respectively analyzed. The levels of serum NSE were measured by electrochemiluminescence at 1st, 3rd,7th days after admission. The bio-chemistry complete set, blood gas analysis, inflammatory markers as well as other biomarkers related to EEG, the Glasgow Coma Scale (GCS), Pediatric Critical Illness Score (PCIS) and the prognosis of the patients were recorded after admission. Results According to the levels of serum initial NSE, they were divided into higher than 64 μg/L group and lower than 64 μg/L group. The prediction accuracy was 90.63%, Youden index was 67.09%, positive likelihood ratio was 14.08. According to the changes of dynamic monitoring of serum NSE, they were divided into A group (NSE values lower than 64 μg/L or initial NSE values higher than 64 μg/L and then quickly decreased ) and B group (Initial NSE reached 64μg/L and then continuously decreased or initial NSE values lower than 64μg/L,peak values higher than 64μg/L). The prediction accuracy was 96.88%, Youden index was 87.61%, positive likelihood ratio was 69.45. NSE lev-els, PCIS scores and GCS scores were significantly different between the groups classified by the different prognosis (P<0.01). Conclusion The concentration of serum NSE can reflect the severity of acute brain injury in critically ill children, is closely related to the prognosis of critically ill children with brain injury. Dynamic monitoring of serum NSE may be essential for controlling the symptoms and prediction of prognosis in critically ill children with brain injury, and has very high value of clinical application.
ABSTRACT
Wilson disease of Progressive Lenticular Degeneration is a familial nervous disease associated with Cirrhosis of the Liver. It has been observed that there is an increased copper content of the liver and brain. Increased excretion of copper in patients with Wilson disease & increased even more after administration of the chelating agent British anti-Lewisite (BAL). Ciruloplasmin, serum protein that binds copper, is reduced. The deposition of copper in tissues is the cause of virtually all the manifestations of the disease in Liver Blood Kidney & Brain We have observed three different cases of different clinical presentations.
ABSTRACT
Objective To study the neurotoxicity of chronic aluminum overload and the protective effects of nimodipine in rats.Methods The brain damage models of rats were established via intragastric administration of aluminum gluconate(element aluminum 400 mg/kg)once a day,5 d/week for 12 weeks.The step-down test and programmed Morris water maze test were used to evaluate the changes of learning and memory functions of rats.Pathomorphological changes of hippocampi of rats were observed.The activities of SOD,ChAT,AchE,MAO-B and the contents of MDA of brain tissue in rats were also measured.Nimodipine(80 mg/kg)were intragastrically administered 4 h after aluminum administration every time for 12 weeks.Results Chronic aluminum administration induced the impairment of avoidance learning and memory ability and spatial oriental ability.Consistent with the behavioral changes,neuronal death in the hippocampi,decreased activities of SOD and ChAT,increased content of MDA,and increased activity of MAO-B and AchE were detected in the aluminum-overload mice.The administration of nimodipine could significantly protect rats from the brain damage,and behavioral and biochemical changes above caused by aluminum overload were in a dose-dependent manner.Conclusion These results suggest that changes of cellular calcium overload and oxide stress and MAO-B activities are involved in pathophysiological mechanisms of brain injury induced by chronic aluminum overload.Nimodipine has a protective effect on neurotoxicity of chronic aluminum overload.