人参二醇组皂苷联合依拉达奉对内毒素休克大鼠心肺损伤的保护作用

目的研究人参二醇组皂苷联合依拉达奉对内毒素休克大鼠心肺损伤保护作用。方法将40只Wistar大鼠随机分为假手术组、模型组、阳性对照组和实验组,每组10只。模型组、阳性对照组和实验组均经股静脉注射大肠杆菌脂多糖(LPS)建立内毒素休克大鼠模型,假手术组注射生理盐水1 mL,建模后,假手术组和模型组经股静脉注射生理盐水0.5 mL,阳性对照组经股静脉注射地塞米松3 mg·kg^-1,实验组经股静脉注射人参二醇组皂苷45 mg·kg^-1+依拉达奉3 mg·kg^-1。给药后4 h后,检测各组大鼠血清酶及肺组织中氧化应激指标水平;用免疫组化法检测各组大鼠肺组织中基质金属蛋白酶-2(MMP-2)及基质金属蛋白酶组织抑制因子-2(TIMP-2)蛋白表达情况;用苏木精-伊红染色法(HE)观察各组大鼠肺组织形态学变化。结果给药后,模型组血清肌酸激酶(CK)、谷草转氨酶(AST)、乳酸脱氢酶(LDH)分别为(1025.12±368.45),(526.48±201.52),(634.58±267.41)U·L^-1,阳性对照组分别为(562.34±211.26),(286.45±232.15),(359.48±105.36)U·L^-1,实验组分别为(389.45±268.47),(252.36±124.51),(298.46±169.74)U·L^-1。阳性对照组和实验组上述指标与模型组相比,差异均有统计学意义(均P<0.01)。模型组大鼠肺组织中MMP-2和TIMP-2分别为0.24±0.06,0.15±0.04,假手术组分别为0.09±0.02,0.14±0.02,阳性对照组分别为0.16±0.04,0.15±0.04,实验组分别为0.18±0.05,0.16±0.03。模型组与假手术组比较,差异均有统计学意义(均P<0.01);实验组和阳性对照组与模型组比较,差异均有统计学意义(均P<0.01)。结论人参二醇组皂苷联合依拉达奉可减轻内毒素休克大鼠肺组织炎性程度,下调肺组织MMP-2表达,同时对心肌也具有一定的保护作用。     

川陈皮素对哮喘大鼠内质网应激信号通路及核苷酸结合寡聚化结构域样受体蛋白3炎症小体活化的影响

目的 探讨川陈皮素(NOB)对哮喘大鼠内质网应激信号通路及核苷酸结合寡聚化结构域样受体蛋白3(NLRP3)炎症小体活化的影响。方法 通过卵清蛋白诱导建立大鼠哮喘模型。将50只造模成功大鼠随机分为低、中、高剂量实验组(分别灌胃100,200和400 mg·kg^-1·d^-1 NOB)、对照组(灌胃5 mg·kg^-1·d^-1地塞米松)、模型组(灌胃等量0.9%NaCl),每组各10只;另选取10只正常大鼠为空白组(灌胃等量0.9%NaCl)。6组大鼠每天灌胃1次,连续10 d。用酶联免疫吸附试验法检测血清中白细胞介素-1β(IL-1β)和肿瘤坏死因子-α(TNF-α)的含量,用蛋白质印迹法检测肺组织中磷酸化C-Jun氨基端激酶(p-JNK)、C/EBP同源蛋白(CHOP)和NLRP3的表达水平。结果 低、高剂量实验组和对照组、模型组、空白组的血清IL-1β分别为(127.25±10.07),(74.32±4.53),(75.64±4.25),(152.33±10.23)和(56.43±3.12)pg·mL...     

灯盏乙素对大鼠瑞舒伐他汀血浆浓度及组织分布的影响

目的考察大鼠体内灯盏乙素对瑞舒伐他汀血浆浓度和组织分布的影响。方法按照体重将大鼠随机分成4组,每组18只:对照组、实验Ⅰ组、实验Ⅱ组和实验Ⅲ组。实验Ⅰ组、实验Ⅱ组和实验Ⅲ组分别灌胃10,50,200 mg·kg-1灯盏乙素,同时均灌胃瑞舒伐他汀5 mg·kg^-1;对照组灌胃等体积0.2%CMC-Na水溶液。分别于给药后1,2,6 h摘眼球取血,取血后立即处死大鼠,取出心、肝、肺、肾、脑组织处理,HPLC-MS测定血浆及组织的瑞舒伐他汀含量。结果所建立的瑞舒伐他汀血浆及组织样本HPLC-MS法符合要求。对照组、实验Ⅰ组、实验Ⅱ组和实验Ⅲ组大鼠的血浆瑞舒伐他汀浓度在1 h分别为(170.38±40.77),(218.09±59.52),(278.64±76.26),(297.48±95.37)ng·m L^-1;在2 h分别为(237.26±70.31),(293.76±89.04),(410.27±102.13),(461.49±121.73)ng·m L^-1;在6 h分别为(131.58±40.52),(166.21±48.52),(236.78±73.40)和(251.33±82.94)ng·m L^-1,各实验组大鼠瑞舒伐他汀血浆浓度高于对照组,差异均有统计学意义(均P<0.05)。各组大鼠的瑞舒伐他汀均主要聚集于肝,对照组、实验Ⅰ组、实验Ⅱ组和实验Ⅲ组在大鼠肝的瑞舒伐他汀浓度在1 h分别为(2098.57±735.10),(1905.91±703.16),(1406.39±435.86),(1217.08±318.65)ng·m L^-1;这4组在2 h分别为(3204.19±893.53),(2863.87±836.12),(2114.28±598.31),(1973.15±512.64)ng·m L^-1;这4组在6 h分别为(1681.71±513.29),(1603.14±517.86),(1120.08±298.75),(1057.91±267.66)ng·m L^-1,实验Ⅱ组和实验Ⅲ组在肝的瑞舒伐他汀浓度低于对照组;实验组Ⅲ组的瑞舒伐他汀在大鼠的心、肺、肾及脑组织的浓度高于对照组,以上差异均有统计学意义(均P<0.05)。结论剂量达到50 mg·kg-1的灯盏乙素对瑞舒伐他汀血浆浓度及肝组织分布均有显著影响,其分布机制可能与竞争蛋白转运体有关。     

麦冬皂苷D调控磷酸酶及张力蛋白同源物诱导激酶1/帕金蛋白通路对脓毒症心肌损伤的保护作用

目的 探讨麦冬皂苷D(OPD)对脓毒症大鼠心肌损伤及磷酸酶及张力蛋白同源物诱导激酶1/帕金蛋白(PINK1/parkin)通路的影响。方法 用盲肠结扎穿孔法构建脓毒症大鼠模型,并将造模成功的大鼠随机分为模型组、实验组、对照组和联合组,每组8只。在模型制备成功后12 h,实验组给予腹腔注射40 mg·kg^-1 OPD,对照组给予腹腔注射20 mg·kg^-1 3-MA,联合组给予腹腔注射40 mg·kg^-1 OPD和20 mg·kg^-1 3-MA;假手术组和模型组均给予腹腔注射等量0.9%NaCl。5组大鼠每12 h重复给药1次,连续给药6 d。用酶联免疫吸附试验法检测血清肌钙蛋白Ⅰ(cTnⅠ)水平,用蛋白质印迹法检测大鼠心肌组织中PINK1和parkin蛋白的表达水平。结果 实验组、对照组、联合组、模型组和假手术组的血清cTnⅠ水平分别为(0.98±0.20)、(3.44±0.69)、(1.64±0.38)、(2.39±0.45)和(0.37±0.07)mg·L^-1,PINK1蛋...     

枸杞多糖对糖尿病性白内障大鼠晶状体上皮细胞热休克蛋白27表达及氧化应激产物的影响

目的探讨枸杞多糖对糖尿病性白内障大鼠晶状体上皮细胞热休克蛋白27(HSP27)表达及氧化应激产物的影响。方法选取健康SD大鼠用链脲佐菌素腹腔注射建立糖尿病性白内障大鼠模型。取15只SD健康大鼠予以等量1mol·L^-1柠檬酸钠缓冲液,作为对照组。将模型大鼠随机分为模型组、实验A组、实验B组,每组16只。实验A组予以12.5 mg·mL^-1氨基胍盐酸盐溶液,每只2 mL;实验B组予以25 mg·m L^-1枸杞多糖溶液,每只2 mL;模型组和对照组均予以灭菌0.9%Na Cl,每只2 mL。4组大鼠均予以灌胃给药或0.9%Na Cl,每天1次,连续给药12周。比较4组大鼠的体重、血糖、晶状体混浊相对灰度值、晶状体氧化应激产物指标水平和晶状体上皮细胞HSP27表达水平。结果治疗后,对照组、模型组、实验A组和实验B组的体重分别为(285.64±19.54),(251.73±10.85),(260.89±11.47)和(270.45±13.11)g,血糖分别为(8.12±0.83),(26.47±3.25),(15.18±1.84)和(10.02±0.43)mmo·L^-1,晶状体混浊相对灰度值分别为(20.28±2.19),(85.66±8.67),(51.18±6.77)和(42.24±5.14),丙二醛分别为(3.95±0.47),(8.15±0.84),(5.73±0.64)和(4.86±0.51)nmol·mg prot^-1,超氧化物歧化酶分别为(75.74±7.64),(33.26±3.18),(54.07±5.72)和(62.78±8.36)U·mg prot^-1,谷胱甘肽过氧化物酶分别为(15.78±1.85),(6.25±0.68),(9.88±1.29)和(13.02±1.14)U·mg prot^-1,HSP27分别为(0.47±0.05),(0.73±0.09),(1.35±0.16)和(1.78±0.22)。模型组、实验A组和实验B组的上述指标与对照组比较,差异均有统计学意义(均P<0.05),且模型组、实验A组和实验B组的上述指标,两两比较,差异均有统计学意义(均P<0.05)。结论枸杞多糖可能通过提高晶状体的抗氧化作用和促进晶状体上皮细胞HSP27表达,来降低糖尿病性白内障大鼠晶状体混浊度,以及改善体重降低和高血糖的情况。     

白藜芦醇对膜性肾病大鼠的肾保护作用

目的研究白藜芦醇对膜性肾病大鼠的肾保护作用及可能的作用机制。方法将SD大鼠随机分为正常组、模型组及实验组,各20只。用尾静脉注射阳离子化牛血清白蛋白(C-BSA)构建膜性肾病大鼠,正常组给予等量生理盐水。建模后实验组灌胃白藜芦醇(30 mg·kg-1),模型组及正常组灌胃等量生理盐水,每天1次,连续干预4周。用分光光度计检测24 h尿蛋白定量(UTP),用试剂盒检测血清中肌酸酐(Scr)、尿素氮(BUN)、白蛋白(ALB)、总胆固醇(TC)指标水平,以免疫组化法检测大鼠肾组织synaptopodin蛋白表达情况,以蛋白质印迹(WB)法检测大鼠肾组织中p-Akt、mTOR、PI3K蛋白表达。结果正常组、模型组和实验组大鼠血清中Scr分别为(29.16±1.77),(52.64±2.78)和(40.55±2.65)μmol·L^-1,BUN分别为(5.86±1.35),(13.54±2.36)和(7.66±3.45)mmol·L^-1,24 h UTP分别为(6.85±1.26),(39.52±1.24)和(25.36±1.42)mg,ALB分别为(32.15±3.49),(19.63±2.48)和(26.34±2.58)g·L^-1,TC分别为(1.26±0.52),(4.02±0.36)和(2.36±0.52)mmol·L^-1,肾组织synaptopodin蛋白表达量分别为(45.36±2.18)%,(12.63±3.85)%,(23.26±3.09)%,差异均有统计学意义(均P<0.05)。模型组肾组织中磷酸化蛋白激酶B(p-Akt)、哺乳动物雷帕霉素靶蛋白(mTOR)、磷脂酰肌醇3-激酶(PI3K)相对表达量较正常组升高,而实验组低于模型组,差异均有统计学意义(均P<0.05)。结论白藜芦醇可减少膜性肾病大鼠尿蛋白程度,防止synaptopodin降解,降低PI3K/Akt/mTOR信号通路中蛋白表达,从而发挥对膜性肾病的肾保护作用。     

白藜芦醇对梗阻性黄疸大鼠肝功能的保护作用

目的研究白藜芦醇对梗阻性黄疸大鼠肝功能的保护作用及相关作用机制。方法用胆总管结扎术的方法建立梗阻性黄疸大鼠模型,将成功构建的梗阻性黄疸大鼠随机分为模型组(n=16)与实验组(n=16),假手术组(n=16)仅开腹游离胆总管但不做结扎。实验组大鼠灌胃白藜芦醇(20 mg·kg^-1·d^-1),假手术组与模型组灌胃等量生理盐水,连续干预2周。用全自动生化分析仪检测大鼠血清谷丙转氨酶(GPT)、谷草转氨酶(GOT)、直接胆红素(DBIL)与总胆红素(TBIL)水平;用苏木精-伊红(HE)染色法观察大鼠肝组织病理学变化;用酶联免疫吸附(ELISA)法检测大鼠血清肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)水平;用蛋白质印迹(Wb)法检测各组大鼠肝组织诱导型一氧化氮合酶(iNOS)、核转录因子-κBp65(NF-кBp65)蛋白的表达水平。结果假手术组、模型组及实验组大鼠血清GPT水平分别为(35.62±7.43),(241.25±19.22),(114.83±6.42)U·L^-1;GOT水平分别为(111.36±12.43),(562.73±48.64),(312.43±19.65)U·L^-1;DBIL水平分别为(7.24±1.32),(263.51±17.22),(141.33±12.52)μmol·L^-1;TBIL水平分别为(9.16±1.43),(342.61±36.84),(181.22±19.86)μmol·L^-1;肝组织iNOS蛋白相对表达量分别为0.15±0.06,0.96±0.04,0.68±0.13;NF-кBp65蛋白相对表达量分别为0.09±0.05,0.73±0.11,0.32±0.12,差异均有统计学意义(均P<0.05)。结论白藜芦醇可有效改善梗阻性黄疸大鼠肝功能生化指标水平,抑制炎症反应,改善肝功能,其作用机制可能与降低肝组织iNOS、NF-кBp65蛋白表达相关。     

白术内酯Ⅰ调控Janus激酶2/信号转导和转录激活因子3通路对分泌性中耳炎大鼠听功能及炎症反应的影响

目的 探究白术内酯Ⅰ调控Janus激酶2(JAK2)/信号转导和转录激活因子3(STAT3)通路对分泌性中耳炎(SOM)大鼠听功能及炎症反应的影响。方法 用卵清蛋白和氢氧化铝致敏构建SOM模型大鼠,并随机分为模型组、联合组和低、高剂量实验组,每组12只;另选12只正常SD大鼠做对照组。低、高剂量实验组分别灌胃给予120和240 mg·kg^-1白术内酯Ⅰ,联合组灌胃给予240 mg·kg^-1白术内酯Ⅰ+21 mg·kg^-1 RO8191;对照组和模型组均灌胃给予等量0.9%NaCl。5组大鼠每天给药1次,连续给药14 d。用听觉脑干诱发电位(ABR)仪检测大鼠听功能(ABR反应阈值),用蛋白质印迹法检测大鼠中耳黏膜组织JAK2/STAT3通路相关蛋白的表达情况。结果 低、高剂量实验组和联合组、模型组、对照组的ABR反应阈值分别为(47.26±5.91)、(26.89±3.75)、(63.37±9.87)、(68.71±10.32)和(24.62±3.53)dB SPL,p-JAK2/JAK2分别为0.48±0.09、0.1...     

黄芪多糖对镉染毒大鼠肾损伤的保护作用

目的探讨黄芪多糖在镉致肾损伤过程中发挥的作用。方法按照随机数字表法将大鼠分为3组,每组12只:空白组、模型组、实验组。模型组和实验组均腹腔注射1.5 mg·kg^-1氯化镉;染毒的同时,实验组给予黄芪多糖20mg·kg^-1,空白组和模型组灌胃等体积0.9%NaCl,干预和染毒每日1次,连续5周。染毒结束后,处死大鼠,摘取大鼠的肾组织,原子吸收分光光度法测定大鼠肾组织的镉(Cd)含量,比色分析法测定大鼠肾组织的超氧化物歧化酶(SOD)活性、乳酸脱氢酶(LDH)活性、谷胱甘肽过氧化物酶(GSH-Px)活性和丙二醛(MDA)含量,ELISA法检测大鼠血清白细胞介素-2(IL-2)含量和转化生长因子-β_1(TGF-β_1)的含量,同时免疫组化法观察肾组织Bcl-2和Bax的蛋白表达。结果空白组、模型组和实验组的IL-2含量分别为(117.38±10.89),(71.82±14.56),(102.46±13.82)pg·mL^-1;这3组的TGF-β_1含量分别为(4.88±0.38),(9.77±0.21),(6.35±0.41)pg·mL^-1;这3组的GSH-Px含量分别为(240.48±18.24),(159.26±21.06),(191.50±23.82)U·g^-1;这3组的LDH含量分别为(1125.25±37.91),(2089.46±35.87),(1159.61±28.86)U·g^-1;这3组的Cd含量分别为(0.02±0.01),(19.68±1.85),(12.99±2.11)mg·kg^-1;这3组的SOD含量分别为(71.55±3.56),(39.30±3.36),(67.25±2.68)U·mg^-1;这3组的MDA含量分别为(3.96±0.79),(7.47±0.78),(5.61±0.99)nmol·mg^-1;这3组的Bcl-2灰度值分别为37.54±3.23,68.43±5.21,38.25±6.17;这3组的Bax灰度值分别为57.87±8.93,27.54±5.45,48.23±3.54。模型组与空白组比较,以上指标差异有统计学意义(均P<0.01);实验组与模型组比较,以上指标差异均有统计学意义(P<0.05或P<0.01)。结论黄芪多糖预处理对镉致大鼠肾氧化损伤存在保护作用,其发挥保护作用是通过调控Bcl-2/Bax蛋白表达实现的。     

白芍总苷通过增加糖尿病大鼠肾组织自噬活性减轻肾损伤的研究

目的 探讨白芍总苷(TGP)对糖尿病大鼠肾组织自噬蛋白Beclin1、微管相关蛋白1轻链3(LC3)表达的影响及肾保护作用。方法 将50只SD大鼠分为正常组10只和造模组40只。造模组用腹腔注射链脲佐菌素建立糖尿病大鼠模型,最终有36只大鼠建模成功,并随机分为模型组和低、高剂量实验组,每组12只。低、高剂量实验组分别灌胃给予100和200 mg·kg^-1·d^-1 TGP;模型组和正常组均灌胃给予同体积0.9%NaCl。4组大鼠每天给药1次,连续给药8周。实验结束时,检测4组大鼠的24 h尿蛋白量、血尿素氮、肌酸酐。用蛋白质印迹法检测大鼠肾组织中Beclin1、LC3-Ⅰ和LC3-Ⅱ蛋白的表达情况。结果 低、高剂量实验组和模型组、正常组的肌酸酐分别为(80.78±7.92)、(73.21±7.54)、(93.05±8.69)和(59.17±6.97)μmol·L^-1,血尿素氮分别为(9.48±1.70)、(8.63±1.38)、(12.20±2.10)和(6.06±0.55)mmol·L^-1,24 h...     

2例利多卡因硬膜外持续镇痛导致排尿困难的病例分析

目的探讨临床药师参与利用利多卡因硬膜外持续镇痛治疗神经病理性疼痛的作用。方法临床药师参与2例利用利多卡因硬膜外持续镇痛治疗神经病理性疼痛的治疗过程,优化用药方案,减少药物不良反应的发生。针对出现类似不良反应患者的药物治疗问题,临床药师通过文献检索获取相关药学信息,结合患者个体情况,为临床治疗提供循证药学支持,同时优化个体给药方案。结果与结论临床药师参与临床工作,从药学的角度提供治疗建议,提高药物治疗疗效,减少药物不良反应的发生。     

Dexamethasone modifies the behavioral effects induced by clonidine in mice

• 1.1. The present study examines the influence of dexamethasone on behavioral effects induced by clonidine in mice.
• 2.2. The behavior elements considered were locomoter activity, rota rod, catalepsy and stereotyped behavior (rearing, grooming, social response test, crossing, smelling, washing face, scratching and bar holding).
• 3.3. Clonidine (0.1-0.5-1.0 mg/kg, IP) induced a significant reduction of all behavioral elements studied when compared to the saline treated group: the behavioral reduction was significant 10 min after administration and lasted for the entire recording period (120 min).
• 4.4. Dexamethasone (0.1-0.5-1.0 mg/kg, IP) per se did not induce significant changes in the behavior elements recorded.
• 5.5. Dexamethasone (0.1-0.5 mg/kg, IP) did not affect behavioral effects induced by the 3 doses of clonidine, whereas the high dose (1 mg/kg) of the steroid significantly reduced its behavioral inhibition.
• 6.6. The results of the present study suggest that dexamethasone induces significant effects on clonidine-induced behavioral effects and that this may be related to an interference with the monoaminergic system.

     

利拉鲁肽注射剂治疗糖尿病的临床研究

目的观察利拉鲁肽治疗糖尿病的临床疗效与安全性。方法选取糖尿病患者86例,随机分为试验组(43例)和对照组(43例)。对照组进行常规治疗。在对照组基础上,试验组于每日早餐前,皮下注射利拉鲁肽0.6 mg,疗程均为24周。比较治疗后2组患者的临床疗效和药物不良反应(ADR),测定2组患者的血糖、脂联素和血管紧张素Ⅱ水平。结果治疗后,试验组总有效率(93.0%)显著高于对照组(76.7%),差异有统计学意义(P<0.05)。治疗后,试验组与对照组的空腹血糖分别为(5.93±0.80),(7.56±0.50)mmol·L^-1;这2组的餐后血糖分别为(7.74±0.76),(9.21±1.06)mmol·L^-1;这2组的糖化血红蛋白分别为(6.02±0.86)%,(8.42±0.50)%,试验组均明显低于对照组,差异均有统计学意义(均P<0.05)。试验组与对照组的脂联素分别为(7.89±0.74),(6.05±0.75)mg·L^-1;这2组的血管紧张素Ⅱ分别为(125.98±2.26),(117.49±4.17)ng·L^-1,试验组的上述指标均明显高于对照组,差异均有统计学意义(均P<0.05)。试验组和对照组ADR发生率分别为0和7.0%,组间差异有统计学意义(P<0.05)。结论利拉鲁肽治疗糖尿病可明显改善机体内各项指标,提高康复率,且安全性较好。     

The index line as a new aid in clinical and forensic toxicology

On behalf of the German Federal Ministry for Research and Technology, we investigated the use of electronic data processing for clinical toxicological purposes. Initially, sufficient funds were available for a comprehensive approach to the problem and programs covering the following areas were established:

1. A casuistic data program;
2. an identification program for wild fruits;
3. a program for the identification of tablets by their shapes

Due to a subsequent lack of funds, it was necessary to develop a partial solution: this solution is what we call the Index Line. The Index Line—limited data on poisonings—should enable the user to receive information by telex from the German Institute for Medical Documentation and Information, i.e., information on “who has what, where”. As a first step the continuous Index Line registration of all cases of poisoning recorded at the poison control centers in Munich, Freiburg, Hamburg, and Nürnberg as well as at the State Institute for Food, Pharmaceutical and Forensic Chemistry in Berlin was founded in 1975. To participate in the program, complete instructions are necessary.     

Dual effects of NMDA-induced intracellular Ca2+ elevations on cGMP levels in cultured cerebellar granule neurons

• 1.1. Cyclic GMP (cGMP) levels were markedly elevated by N-methyl-d-aspartate (NMDA) within 1–3 min of incubation, then gradually decreased with incubation time.
• 2.2. The NMDA-induced intracellular Ca²⁺ elevations showed maximal levels just after adding NMDA and were maintained for 60 min.
• 3.3. NMDA did not show augmentation of cGMP elevation with sodium nitroprusside (SNP), rather it decreased the SNP-induced cGMP elevation after exposure for 60 min.
• 4.4. The NMDA-induced elevation of cGMP was remarkably augmented with the phosphodiesterase inhibitor, 3-isobutyl-l-methylxanthine (IBMX, 1mM), after 60 min of incubation.

     

培美曲塞注射剂联合顺铂注射剂治疗非小细胞肺癌的临床疗效研究

目的观察培美曲塞注射剂联合顺铂注射剂治疗非小细胞肺癌的临床疗效及安全性。方法将42例非小细胞肺癌患者随机分为对照组21例和试验组21例。对照组予以静脉滴注500 mg·m^-2培美曲塞(第1天);试验组予以静脉滴注500 mg·m^-2培美曲塞(第1天),30 min后,静脉滴注25 mg·m^-2顺铂(第1~3天)。2组患者1个疗程均为3周,共治疗2个疗程。比较2组患者的临床疗效和药物不良反应的发生情况。结果治疗后,试验组和对照组的总有效率分别为52.38%(11例/21例)和23.81%(5例/21例),差异有统计学意义(P<0.05)。试验组发生的药物不良反应为发热,对照组发生的药物不良反应有血小板减少、发热和皮疹。试验组和对照组的总药物不良反应发生率分别为47.62%和57.14%,差异无统计学意义(P>0.05)。结论培美曲塞注射剂联合顺铂注射剂治疗非小细胞肺癌的临床疗效确切,且不增加药物不良反应的发生率。     

帕利哌酮缓释片治疗精神分裂症的临床研究

目的观察帕利哌酮缓释片治疗精神分裂症的临床疗效及和安全性。方法将30例精神分裂症患者随机分为对照组15例和试验组15例。对照组予以口服奥氮平,起始剂量10 mg,最高剂量20 mg,bid;试验组予以早上口服帕利哌酮缓释片3 mg,qd,并根据患者症状按3 mg·d-1增加剂量,最大剂量为12mg。2组患者均治疗8周。比较2组患者的临床疗效、心肌酶谱、执行功能,以及药物不良反应的发生情况。结果治疗后,试验组和对照组的总有效率分别为93.33%(14例/15例)和60.00%(9例/15例),差异有统计学意义(P<0.05)。治疗后,试验组和对照组的碱性磷酸酶分别为(72.51±8.82)和(83.24±9.15)U·L^-1,α-羟丁酸脱氢酶分别为(128.66±15.42)和(142.13±12.65)U·L^-1,肌酸磷酸激酶分别为(56.37±8.29)和(62.15±6.45)mmol·L^-1,乳酸脱氢酶分别为(51.35±6.37)和(58.32±6.15)mmol·L^-1,肌酸激酶同工酶分别为(4.15±2.40)和(5.86±0.87)mmol·L^-1,威斯康星卡片分类测验持续性错误数分别为(6.13±0.85)和(5.08±0.68)次,执行功能行为评定量表评分分别为(66.82±8.46)和(55.68±6.24)分,差异均有统计学意义(均P<0.05)。2组患者均未发生药物不良反应。结论帕利哌酮缓释片治疗精神分裂症的临床疗效显著,可显著改善患者的心肌功能,提高执行功能,且安全性较高。     

Beraprost sodium protects occlusion/reperfusion injury in the dog by inhibition of neutrophil migration

• 1.1. The effects of beraprost sodium (beraprost) on myocardial infarct size in an anesthetized open-chest canine model of regional myocardial ischemia and reperfusion were investigated.
• 2.2. Administration of beraprost (300 ng/kg/min, intravenously) to dogs 45 min after left circumflex coronary artery occlusion until 105 min after reperfusion resulted in a significant reduction in infarct size.
• 3.3. The values of control and beraprost treated infarct size expressed as a percentage of the total left ventricle were 15 ± 3% and 4 ± 2%, respectively.
• 4.4. Reperfusion arrythmia, plasma creatine phosphokinase (CK) and lactate dehydrogenase (LDH) level were significantly suppressed by treatment with beraprost.
• 5.5. By histological examination, beraprost proved to reduce neutrophil migration in the ischemic myocardium after 5 h reperfusion.
• 6.6. Therefore, it is suggested that the cytoprotective effect of beraprost during myocardial ischemia and reperfusion may be the consequence of the inhibition of neutrophil migration.

     

Vasoconstrictor-mediated release of purines and pyrimidines from perfused rat hindlimb,perfused mesenteric arcade and incubated de-endothelialized aorta

• 1.1. Reperfusion of hindlimbs that had previously been exposed to either 10 or 60 min global ischaemia resulted in transient washouts of uracil and uric acid in approximate proportion to the interval of ischaemia. However, changing the interval of sequential angiotensin II infusions from 10 to 60 min did not affect the magnitude of sustained uracil and uric acid release.
• 2.2. Perfused rat mesenteric artery arcade released uracil and uric acid and each was further increased approximately 2-fold by exposure to the vasoconstrictor, serotonin (6.7 μM).
• 3.3. Incubated de-endothelialized rat aorta also released purines and pyrimidines and this was increased further when subjected to increased work loads.
• 4.4. The increased rates of release of purines and pyrimidines from hindlimb, and the simpler vascular preparations of mesenteric arcade and aorta, were in proportion to the relative rates of increase in oxygen consumption under maximum vascular load.
• 5.5. It is concluded that the release of purine and pyrimidine nucleosides and their catabolites from perfused rat hindlimb occurring as a consequence of vasoconstriction is not the result of release from previously ischaemic tissue. In addition, release of purines and pyrimidines appears to be a general feature of vascular smooth muscle subjected to high workloads.

     

Kainate produces concentration-dependent elevation of glutamate release but not cGMP levels in cultured neuron

• 1.1. Treatment of cultured cerebellar granule cells for 3 min with N-methyl-D-aspartate (NMDA) resulted in a concentration-dependent elevation of cyclic GMP. However, neither kainate (KA) nor NMDA produced a concentration-dependent elevation of this nucleotide after exposing cells to the agonist for 60 min.
• 2.2. Unlike the case for cGMP, both KA and NMDA produced concentration-dependent elevations of glutamate for 60 min incubation.
• 3.3. The NMDA-induced elevations of cGMP and glutamate were blocked by selective NMDA receptor antagonists.
• 4.4. The selective KA/α-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA) receptor antagonist, 6,7-nitroquinoxaline-2,3-dione (DNQX), blocked the KA-induced elevations of cGMP with 3-min exposures, but it augmented the response with 60-min exposures. However, the KA-induced release of glutamate was prevented by DNQX.
• 5.5. The KA/AMPA receptor antagonist, GYKI 52466, blocked all KA-induced responses regardless of the incubation times.