Objective To investigate the regulatory effect of branched chain amino acids (BCAA) on the expression of apoptosis related proteins after cerebral ischemia reperfusion injury and the protective effects of BCAA on ischemic brain injury in rats.Methods 40 male SD rats were randomly divided into normal diet group (n =20) and branched chain amino acid (BCAA) group (n=20) according to the random number table,and each group was randomly divided into control group (n=6),sham operation group (n=6) and model group (n =8) which used suture method to make ischemia reperfusion model.After modeling,modified Neurological Severity Scores (mNSS) was used to access the neurological impairment degree of 2,6,24,48 and 72 h in each group.The expression of apoptosis related proteins (Cleaved,Bax/Bcl-2) after 72 h was detected by the method of immune protein imprinting (Caspase3) and compared between normal diet group and BCAA group.Results Compared with the normal diet rats,the mNSS of BCAA diet rats after modeling at 2,6,24,48,72 h decreased (11.35±2.78 vs.7.15±2.41,P=0.019;9.35±1.75 vs.5.82±1.17,P=0.002;6.11±1.16vs.4.39±1.46,P=0.048;5.87±1.32vs.3.55±1.94,P=0.036;4.98±2.24vs.2.09±1.33,P=0.022).The expression of cleaved caspase3 protein and the ratio of Bax/Bcl-2 decreased in BCAA group.Conclusion BCAA can alleviate the apoptosis of rats after ischemia and reperfusion,reduce the damage of nerve function,and has a positive protective effect on ischemic brain injury.

Objective:To investigate the clinical features, diagnosis, and treatment of the central nervous system (CNS) toxicity caused by bortezomib.Methods:This study reports five new cases of CNS toxicity caused by bortezomib to elucidate its characteristics along with a review of the literature.Results:CNS toxicity caused by bortezomib presents in three clinical forms: syndrome of inappropriate antidiuresis (SIAD) , posterior reversible encephalopathy syndrome (PRES) , and central fever, which is the most common clinical manifestation. Four of our five patients developed central fever after the administration of bortezomib, manifested as persistent high fever, anhidrosis, and absence of infective foci; the symptom could be improved by discontinuance of bortezomib. Of these patients, three concurrently presented with refractory hyponatremia and one was clearly diagnosed with SIAD. The bortezomib could have caused damages to the hypothalamus and induced both central fever and SIAD. In addition, one patient was diagnosed with PRES due to disturbance of consciousness and epilepsy after taking bortezomib. After discontinuation of bortezomib, the symptoms disappeared and did not recur. We also found that thrombocytopenia may be related to the severity of the CNS toxicity of bortezomib.Conclusion:Cases of CNS toxicity of bortezomib are extremely rare and present as SIAD, PRES and central fever. Early detection and treatment of bortezomib are very important to prevent irreversible neurological complications.