Pathogenesis of acute stroke and the role of inflammasomes

Inflammation is an innate immune response to infection or tissue damage that is designed to limit harm to the host, but contributes significantly to ischemic brain injury following stroke. The inflammatory response is initiated by the detection of acute damage via extracellular and intracellular pattern recognition receptors, which respond to conserved microbial structures, termed pathogen-associated molecular patterns or host-derived danger signals termed damage-associated molecular patterns. Multi-protein complexes known as inflammasomes (e.g. containing NLRP1, NLRP2, NLRP3, NLRP6, NLRP7, NLRP12, NLRC4, AIM2 and/or Pyrin), then process these signals to trigger an effector response. Briefly, signaling through NLRP1 and NLRP3 inflammasomes produces cleaved caspase-1, which cleaves both pro-IL-1β and pro-IL-18 into their biologically active mature pro-inflammatory cytokines that are released into the extracellular environment. This review will describe the molecular structure, cellular signaling pathways and current evidence for inflammasome activation following cerebral ischemia, and the potential for future treatments for stroke that may involve targeting inflammasome formation or its products in the ischemic brain.     

Potential advantages of a combination of Chinese Medicine and bone marrow mesenchymal stem cell transplantation for removing blood stasis and stimulating neogenesis during ischemic stroke treatment

Combined treatment of ischemic stroke with Chinese medicine and exogenous bone marrow mesenchymal stem cell (BMSC) transplantation may improve the removal of blood stasis and stimulation of neogenesis.Chinese medicines that remove blood stasis not only promote blood circulation but also calm the endopathic wind,remove heat,resolve phlegm,remove toxic substances and strengthen body resistance.The medicinal targeting effect of Chinese medicine can promote the homing of BMSCs,and the synergistic therapeutic effects of drugs can contribute to BMSC differentiation.As such,exogenous BMSC transplantation has potential advantages for neogenesis.Chinese medicines and exogenous BMSCs provide complementary functions for the removal of blood stasis and stimulation of neogenesis.Therefore,a combination of Chinese medicine and transplantation of exogenous BMSCs may be particularly suited to ischemic stroke treatment.     

不同剂量辛伐他汀对缺血性脑血管患者脑血管储备能力的影响

目的：研究不同剂量辛伐他汀对缺血性脑血管患者脑血管储备能力的影响。方法将90例缺血性脑血管患者分为常规组、强化组和对照组。对照组患者口服拜阿司匹林，对症治疗；常规组患者服用常规剂量辛伐他汀治疗；强化组服用强化剂量辛伐他汀治疗。检测比较患者治疗前后的脑血管储备能力。结果治疗6个月后，常规组屏气指数为1·21±0·13，脑血管储备能力为30·44±5·09；强化组屏气指数为1·54±0·11，脑血管储备能力为36·14±5·13；对照组的屏气指数为0·95±0·11，脑血管储备能力为21·42±5·20。3组患者的屏气指数和脑血管储备能力较治疗前均有一定程度增加，但强化组增加的幅度最明显。结论强化剂量的辛伐他汀对患者CVR有较好疗效。     

Potential advantages of a combination of Chinese Medicine and bone marrow mesenchymal stem cell transplantation for removing blood stasis and stimulating neogenesis during ischemic stroke treatment

Combined treatment of ischemic stroke with Chinese medicine and exogenous bone marrow mesenchymal stem cell(BMSC) transplantation may improve the removal of blood stasis and stimulation of neogenesis.Chinese medicines that remove blood stasis not only promote blood circulation but also calm the endopathic wind,remove heat,resolve phlegm,remove toxic substances and strengthen body resistance.The medicinal targeting effect of Chinese medicine can promote the homing of BMSCs,and the synergistic therapeutic effects of drugs can contribute to BMSC differentiation.As such,exogenous BMSC transplantation has potential advantages for neogenesis.Chinese medicines and exogenous BMSCs provide complementary functions for the removal of blood stasis and stimulation of neogenesis.Therefore,a combination of Chinese medicine and transplantation of exogenous BMSCs may be particularly suited to ischemic stroke treatment.     

侯氏黑散治疗缺血性中风的理论探析

侯氏黑散出自《金匮要略》,具有祛风化痰、补虚除热、祛瘀通络之功。然而历代医家对其认识不一,通过对此方进行方义阐释,分析侯氏黑散与缺血性中风的关系,结合临床验案,笔者认为此方属于仲景博采众方所录,病机为心脾气血亏虚,风痰阻络,为内外风同治之方,临床用于缺血性中风的预防与治疗,疗效显著。     

缺血修饰白蛋白在运动压力测试中的应用探讨

目的评估冠状动脉疾病患者进行运动压力测试后血液中缺血修饰白蛋白的水平。方法选取本院49例一周内出现胸痛的患者，进行冠脉造影与单车运动压力测试，采集开始运动测试时的血液样本测试缺血修饰白蛋白，作为基线水平，5分钟后再次采样测试缺血修饰白蛋白水平。结果49例患者中，共中有25例（冠状动脉疾病组）有冠状动脉狭窄，另外24例（非冠状动脉疾病组）无冠状动脉狭窄。而缺血修饰白蛋白水平在基线水平与运动水平并无差异，冠状动脉疾病纽与非冠状动脉疾病组基线水平分别为70．7±7．2U／mL、72．5±6．4U／mL，而运动后水平为74．1±5．1、75．8±6．8U／mL，冠状动脉疾病组与非冠状动脉疾病组对比结果分别为P=0．28，P=0．55，二者无明显统计学差异。同时在运动后缺血修饰白蛋白水平变化值两组分别为5．4±3．5、4．7±7．6U／mL，P=0．10；同样的，在心电图阳性组（16例）与心电图阴性组（33例）缺血修饰白蛋白水平变化也无明显差异（6．6±3．IU／mL、7．50±4．2U／mL，P=0．15）。结论缺血修饰白蛋白在运动测试中对于急性冠脉综舍症的诊断并不适用。     

中药药氧疗法联合黛力新治疗缺血性脑卒中后抑郁状态临床研究

目的:观察中药药氧疗法联合黛力新治疗缺血性脑卒中后抑郁状态的临床疗效。方法:将100例患者随机分为观察组和对照组,每组50例。对照组给予口服黛力新治疗,观察组在对照组基础上予以中药药氧疗法治疗。分别于治疗前、治疗6周后采用汉密尔顿抑郁量表(Hamilton depression scale for depression,HAMD)(24项)评估患者治疗后抑郁状态的严重程度,脑卒中生活质量量表(stroke-specific quality of life,SS-QOL)评价患者的生活质量;观察患者治疗过程中的各种不良反应,评价临床疗效。结果:治疗后观察组HAMD评分、SS-QOL评分均明显低于对照组,差异有统计学意义(P0.01)。观察组有效率为88.00%,对照组有效率68.00%,两组比较,差异有统计学意义(P0.01)。两组患者治疗过程中均未出现严重不良反应,两组比较,差异无统计学意义(P0.05)。结论:中药药氧疗法与黛力新联合应用可改善缺血性脑卒中患者的抑郁情绪,增强治疗效果,提高患者生活质量。     

CO-ADMINISTRATION OF FUROSEMIDE AUGMENTS TACROLIMUS-INDUCED IMPAIRMENT IN KIDNEY FUNCTION IN RATS

Sodium-depletion in rats reproduces functional and morphological tacrolimus nephrotoxicity observed in man. Potent diuretics induce sodium-depletion. Our objective was to determine the effect of a loop diuretic furosemide on tacrolimus-mediated functional and pathological impairment of the kidney in rats. Sprague-Dawley rats were divided into four groups; group 1, rats received vehicle (saline) only; group 2, rats were treated with tacrolimus (1mg/kg body weight) and furosemide (5mg/kg body weight); group 3, rats were treated with tacrolimus alone; and group 4, rats were treated with furosemide (5mg/kg body weight) alone. On day 28, tail blood pressure was measured and the rats were placed in metabolic cages for urine collection. After 24 hr the rats were sacrificed. Tacrolimus alone tended to cause growth retardation, hypotension, hypomagnesemia and a rise in blood urea nitrogen. Furosemide co-administration enhanced the effects of tacrolimus on hypotension, hypomagnesemia and a rise in blood urea nitrogen. The renal histology characterized by cytoplasmic vacuolization of the proximal tubules was not different between the rats treated with both tacrolimus and furosemide and the rats treated with tacrolimus alone. A strong immunostaining for FKBP-12, a tacrolimus-binding protein, was observed in the medulla of the kidneys of rats treated with tacrolimus either with or without furosemide.These results indicate that furosemide further augments tacrolimus induced impairment in kidney function, and that furosemide should be used with discretion in patients on tacrolimus therapy.