Salvianolic acid A prevented cerebrovascular endothelial injury caused by acute ischemic stroke through inhibiting the Src signaling pathway

Stroke is an acute cerebrovascular disease caused by ruptured or blocked blood vessels.For the prevention of ischemic stroke,the coagulation state of blood and cerebrovascular protection should be considered.Our previous study has shown that salvianolic acid A(SAA),which is a water-soluble component from the root of Salvia Miltiorrhiza Bge,prevents thrombosis with a mild inhibitory effect on platelet aggregation.In this study we investigated the preventive effects of SAA on cerebrovascular endothelial injury caused by ischemia in vivo and oxygen-glucose deprivation(OGD)in vitro,and explored the underlying mechanisms.An autologous thrombus stroke model was established in SD rats by electrocoagulation.SAA(10 mg/kg)was orally administered twice a day for 5 days before the operation.The rats were sacrificed at 24 h after the operation.We showed that pretreatment with SAA significantly improved the neurological deficits,intracerebral hemorrhage,BBB disruption,and vascular endothelial dysfunction as compared with model group.In human brain microvascular endothelial cells(HBMECs),pretreatment with SAA(10μM)significantly inhibited OGD-induced cell viability reduction and degradation of tight junction proteins(ZO-1,occludin,claudin-5).Furthermore,we found that SAA inhibited the upregulation of Src signaling pathway in vivo and vitro and reversed the increased expression of matrix metalloproteinases(MMPs)after ischemic stroke.In conclusion,our results suggest that SAA protects cerebrovascular endothelial cells against ischemia and OGD injury via suppressing Src signaling pathway.These findings show that pretreatment with SAA is a potential therapeutic strategy for the prevention of ischemic stroke.     

狂犬病诊治进展

人类的狂犬病是一种中枢神经系统病毒感染性疾病,常由患狂犬病动物的唾液污染伤口而传染;一旦出现症状,病人基本上100%死亡,从狂犬病后康复的病例极为罕见,仅有3例报道。临床表现为特有的恐水怕风、咽肌痉挛、进行性瘫痪等。狂犬病在87个国家有流行,主要流行于东南亚、非洲及拉     

苯扎溴铵溶液的稳定性观察

目的:评价在常温和0℃下存放的苯扎溴铵(新沽尔灭)的杀茵效果.方法:采用厂家3个批号的苯扎溴铵,分别于常温和0℃下存放24 h.稀释成1:50浓度后,将3种标准菌株置于其中,分别在作用5,10,15,30,60,120 min后取出药液,倾入培养基,置35℃培养箱培养48 h,观察菌株的存活情况.结果:经两种温度、不同时间的菌株培养结果观察,苯扎溴铵的杀菌效果一致,均能快速杀灭3种标准菌株.结论:苯扎溴铵消毒液保存在0℃下,不影响其杀菌效力,只要在保质期内,结冰的消毒液仍可使用,其性能稳定.     

布洛芬对乙酰氨基酚退热疗效对比

长期以来,发热是儿科关注的问题,发热程度有助于判断病情,儿童多因与病情不成比例,轻微疾病即可出现发烧,父母常常不了解这一现象而引起不必要的恐慌,随意应用退热药即成为儿科普遍的现象[1].采用安全有效的退热药物值得临床探讨.     

Neural circuits and nicotinic acetylcholine receptors mediate the cholinergic regulation of midbrain dopaminergic neurons and nicotine dependence

Midbrain dopaminergic(DA)neurons are governed by an endogenous cholinergic system,originated in the mesopontine nuclei.Nicotine hijacks nicotinic acetylcholine receptors(nAChRs)and interferes with physiological function of the cholinergic system.In this review,we describe the anatomical organization of the cholinergic system and the key nAChR subtypes mediating cholinergic regulation of DA transmission and nicotine reward and dependence,in an effort to identify potential targets for smoking intervention.Cholinergic modulation of midbrain DA systems relies on topographic organization of mesopontine cholinergic projections,and activation of nAChRs in midbrain DA neurons.Previous studies have revealed thatα4,α6,andβ2 subunit-containing nAChRs expressed in midbrain DA neurons and their terminals in the striatum regulatefirings of midbrain DA neurons and activity-dependent dopamine release in the striatum.These nAChRs undergo modification upon chronic nicotine exposure.Clinical investigation has demonstrated that partial agonists of these receptors elevate the success rate of smoking cessation relative to placebo.However,further investigations are required to refine the drug targets to mitigate unpleasant side-effects.     

Establishment of a mouse model of cancer cachexia with spleen deficiency syndrome and the effects of atractylenolide I

Cancer cachexia is a multifactorial metabolic syndrome that affects～50%–80%of cancer patients,and no effective therapy for cancer cachexia is presently available.In traditional Chinese medicine,a large portion of patients with cancer cachexia was diagnosed as spleen deficiency syndrome and treated with tonifying TCMs that produce clinic benefits.In this study we established a new animal model of spleen deficiency and cancer cachexia in mice and evaluated the therapeutic effects of atractylenolide I,an active component of tonifying TCM BaiZhu,in the mouse model.Cancer cachexia was induced in male BALB/c mice by inoculation of mouse C26 colon adenocarcinoma cells,whereas spleen deficiency syndrome was induced by treating the mice with spleen deficiency-inducing factors,including limited feeding,fatigue,and purging.The mouse model was characterized by both cachexia and spleen deficiency characteristics,including significant body weight loss,cancer growth,muscle atrophy,fat lipolysis,spleen,and thymus atrophy as compared with healthy control mice,cancer cachexia mice,and spleen deficiency mice.Oral administration of atractylenolide I(20 mg·kg?1per day,for 30 days)significantly ameliorated the reduction in body weight and atrophy of muscle,fat,spleen,and thymus in mice with spleen deficiency and cachexia.The established model of spleen deficiency and cancer cachexia might be useful in the future for screening possible anticachexia TCMs and clarifying their mechanisms.     

春季食养贵在肝脾

主持人的话 过了立春和春节,大地开始逐渐由寒变暖.这就预示着春暖花开的季节即将来到了. 从立春到立夏前,包括立春、雨水、惊蛰、春分、清明、谷雨6个节气,是生发的季节.这段时间,春归大地,阳气生发,冰雪消融,蛰虫苏醒,自然界生机勃发,一派欣欣向荣的景象.此时养生,需适应季节变化,使机体与外界统一起来.中医称之为"春气之应,养生之道也".     

抢救儿童有机磷中毒21例临床体会

<正>有机磷农药可因食入、吸入或皮肤吸收而中毒。小儿中毒原因多为:误食被有机磷农药污染的食物;误用污染农药的玩具或农药容器;母亲在使用农药后未认真洗手及换衣服而给婴儿哺乳,不恰     

对于自杀,一个就太多了

"活着"是每个人至高无上的权利,可有些人偏偏选择了放弃。9月是开学的日子,文文告别了父母兄妹,揣着东挪西凑的学费上了北京。她是乡里第一个考上北京名牌大学的学生,全乡人都以她为自豪。同宿舍的女生都来自城里,一个个时尚、新潮。看着她     

由中、英、法药品监管现状的比较看我国的中药监管

为进一步了解英、法等发达国家的药品监管体系,借鉴其在药品监管信息化建设方面的成功经验,北京市药品监督管理局东城分局与北京市科学技术委员于不久前赴英国、法国实地考察,并与英国药理学会(British Pharmacological Society)、法国退休专家志愿者协会(France Volunteer Association of the Retired Experts)进行了深入的交流.     

糖酵解抑制剂抗癫痫机制的新研究进展

神经细胞兴奋性的代谢调节作为控制癫痫发作的一个重要因素已经逐步被认识到。糖酵解抑制剂生酮饮食、2-脱氧葡萄糖、1,6-二磷酸果糖通过降低神经细胞的兴奋性从而发挥抗癫痫作用,其疗效在临床上已经明确,但是其具体抗癫痫机制尚不完全清楚。本文对其抗癫痫机制的新研究进展进行综述。     

Anaesthetic agents and glycolysis

Summary The influence of halothane, chloroform and propanidid on hexokinase, phosphoglucose-isomerase and phosphofructokinase was studied in vitro. None of the three anaesthetic agents significantly inhibited the activity of hexokinase or phosphoglucose-isomerase preparations.A significant inhibition of phosphofructokinase was brought about by halothane, chloroform and propanidid.The inhibitory effect proved to be dependent upon the concentration of the anaesthetic drugs. It is unlikely that the resulting weak inhibition of glycolysis is causally related to the acute cardiodepressive action of the anaesthetic agents studied. However, the inhibition of glucose oxidation by halothane and other potent anaesthetic agents might be harmful after prolonged exposure, especially since significant accumulation in cardiac and other tissues occurs.     

Actions of quercetin on gluconeogenesis and glycolysis in rat liver

1. The action of quercetin on glucose catabolism and production was investigated in the perfused rat liver. 2. Quercetin inhibited lactate production from glucose: 80% inhibition was found at a quercetin concentration of 100 µM, and at higher concentrations inhibition was complete. 3. Pyruvate production from glucose presented a complex pattern, but stimulation was evident at 100 and 300 µM quercetin. Oxygen uptake tended to be increased. 4. Glucose synthesis from lactate and pyruvate was inhibited. Inhibition was already evident at 50 µM quercetin and almost complete at 300 µM. Concomitantly, the increment in oxygen uptake caused by lactate plus pyruvate was stimulated by 50 µM quercetin, but clearly inhibited by higher concentrations (100-500 µM). 5. Glucose phosphorylation in the high-speed supernatant fractions of liver homogenates was inhibited by quercetin, but only at concentrations above 150 µM. 6. It is concluded that quercetin can inhibit both glucose degradation and production and increase the cytosolic NAD + /NADH ratio. 7. These effects are likely to arise from many causes. Reduction of oxidative phosphorylation, inhibition of Na + -K + -ATPase, inhibition of glucokinase and inhibition of glucose 6-phosphatase could all contribute to the overall action of quercetin.     

Actions of quercetin on gluconeogenesis and glycolysis in rat liver

1. The action of quercetin on glucose catabolism and production was investigated in the perfused rat liver. 2. Quercetin inhibited lactate production from glucose: 80% inhibition was found at a quercetin concentration of 100 micro M, and at higher concentrations inhibition was complete. 3. Pyruvate production from glucose presented a complex pattern, but stimulation was evident at 100 and 300 micro M quercetin. Oxygen uptake tended to be increased. 4. Glucose synthesis from lactate and pyruvate was inhibited. Inhibition was already evident at 50 micro M quercetin and almost complete at 300 micro M. Concomitantly, the increment in oxygen uptake caused by lactate plus pyruvate was stimulated by 50 micro M quercetin, but clearly inhibited by higher concentrations (100-500 micro M). 5. Glucose phosphorylation in the high-speed supernatant fractions of liver homogenates was inhibited by quercetin, but only at concentrations above 150 micro M. 6. It is concluded that quercetin can inhibit both glucose degradation and production and increase the cytosolic NAD(+)/NADH ratio. 7. These effects are likely to arise from many causes. Reduction of oxidative phosphorylation, inhibition of Na(+)-K(+)-ATPase, inhibition of glucokinase and inhibition of glucose 6-phosphatase could all contribute to the overall action of quercetin.     

Effect of tremorine and oxotremorine on aerobic glycolysis in rat brain

Tremorine and oxotremorine at concentrations from 5 × 10⁻⁸ to 5 × 10⁻⁴ M stimulated aerobic glycolysis in slices of rat brain cortex. The addition of atropine blocked this stimulation. Acetylcholine in concentrations from 5 × 10⁻⁸ to 5 × 10⁻⁶ M failed to alter the rate of glycolysis in slices of cortex, but it inhibited glycolysis in concentrations of 5 × 10⁻⁵ and 5 × 10⁻⁴ M. In homogenates of rat brain cortex tremorine, oxotremorine and acetylcholine elicited no effect on aerobic glycolysis.