利拉鲁肽通过调节Sestrin2改善棕榈酸诱导的L6骨骼肌细胞胰岛素抵抗

目的探讨应激诱导蛋白Sestrin2(Sesn2)在利拉鲁肽改善大鼠L6骨骼肌细胞胰岛素抵抗中的作用。方法采用棕榈酸诱导法建立大鼠L6骨骼肌细胞的胰岛素抵抗, 将实验细胞分为对照组(Con组)、棕榈酸0.6 mmol/L处理组(PA组)、棕榈酸0.6 mmol/L+利拉鲁肽10 nmol/L处理组(PA+Lir10组)、棕榈酸0.6 mmol/L+利拉鲁肽100 nmol/L处理组(PA+Lir100组)和棕榈酸0.6 mmol/L+利拉鲁肽1 000 nmol/L处理组(PA+Lir1000组)。细胞计数试剂盒8(CCK8)法检测各组细胞活性, Western印迹法检测各组葡萄糖转运蛋白4(GLUT4)、蛋白激酶B(Akt)、磷酸化的蛋白激酶B(p-Akt)和Sesn2蛋白的表达。小干扰RNA(siRNA)转染L6细胞, 抑制Sesn2的表达后, 用棕榈酸0.6 mmol/L和利拉鲁肽100 nmol/L干预细胞, 采用Western印迹法检测细胞中Sesn2、Akt、p-Akt、GLUT4蛋白表达水平。结果与Con组相比, PA组细胞存活率明显下降(P<0.05), p-Ak...     

利拉鲁肽和达格列净治疗超重及肥胖2型糖尿病患者的疗效及安全性比较

目的比较利拉鲁肽和达格列净均联合二甲双胍治疗超重及肥胖T2DM患者的疗效及安全性。方法选取2018年1月至2020年9月于香港大学深圳医院内分泌科门诊及住院治疗的213例BMI25 kg/m~2的T2DM患者,依据不同治疗方式分为利拉鲁肽组(Lir组)106例和达格列净组(Dap组)107例。治疗24周后,比较两组治疗前后FPG、HbA1c和其他生化指标,记录观察期间不良反应发生情况。结果与同组治疗前比较,两组治疗后体重(BW)、WC、SBP、DBP、FPG、HbA_1c、TC、TG、LDL-C、血尿酸均降低(P0.05)。Dap组治疗后BW、WC高于Lir组,SBP低于Lir组(P0.05)。Dap组上消化道不良反应低于Lir组(P0.05)。Dap组泌尿生殖道感染、酮症增加(P0.05),且出现血糖正常的DKA。两组间总不良反应发生率比较,差异无统计学意义。结论利拉鲁肽联合二甲双胍与达格列净联合二甲双胍对超重及肥胖T2DM患者的降糖效果相当,利拉鲁肽降低BW和WC的幅度更大,达格列净能更有效地降低患者SBP。利拉鲁肽治疗后上消化道不良反应较多,达格列净泌尿生殖道感染及DKA风险需引起注意。     

利拉鲁肽治疗新诊断2型糖尿病患者临床疗效的观察

目的观察利拉鲁肽治疗新诊断T2DM患者的临床疗效。方法 48例新诊断T2DM患者被随机分为利拉鲁肽组和二甲双胍组,每组各24例。结果治疗12周后,两组FPG、2hPG、HbA1c、体重、HOMA-IR及血脂等差异均有统计学意义(P0.01),利拉鲁肽组优于二甲双胍组(P0.05),且治疗后利拉鲁肽组FC-P、2hC-P水平升高(P0.01)。结论利拉鲁肽用于治疗新诊断T2DM患者,安全有效。     

芪参益气滴丸对正常家兔血小板胞浆内游离钙浓度的影响

目的研究芪参益气滴丸对正常家兔血小板胞浆游离钙浓度[Ca~(2+)]i的影响。方法以Fura-2/AM荧光分光光度法测定家兔血小板内[Ca~(2+)]i的变化。结果对照组的血小板[Ca~(2+)]i为(217.020 4±94.399 4)nmol/L,芪参益气滴丸小剂量组血小板[Ca~(2+)]i为(197.152 5±89.574 3)nmol/L,中剂量组为(120.680 2±71.452 6)nmol/L,大剂量组为(84.849 0±26.335 9)nmol/L。与对照组相比,芪参益气滴丸不同剂量组均能够降低正常大鼠血小板[Ca~(2+)]i。不同剂量的芪参益气滴丸与血小板[Ca~(2+)]i之间呈线性相关。结论推测芪参益气滴丸的益气活血通脉作用可能与其降低血小板内[Ca~(2+)]i相关。     

利拉鲁肽治疗与恩格列净治疗超重/肥胖2型糖尿病患者的疗效比较

目的观察利拉鲁肽治疗的超重/肥胖T2DM患者改用恩格列净治疗后的疗效。方法选取136例经利拉鲁肽治疗26周的超重/肥胖T2DM患者,随机分为利拉鲁肽组(Lir)46例、恩格列净组(Emp)46例及阿卡波糖组(Aca)44例,继续治疗26周。比较各组治疗前后血糖、体重、BMI、WC、BP、血尿酸(SUA)、血脂及肝肾功能。结果 Lir、Emp组治疗前后体重、BMI、WC及BP比较,差异无统计学意义(P0.05)。与同组治疗前比较,Lir组LDL-C降低,HDL-C升高(P0.05或P0.01);Emp组SUA降低(P0.01);Aca组体重、BMI、WC、SBP升高(P0.01)。与Aca组治疗后比较,Lir、Emp组治疗后体重、BMI、WC、SBP降低(P0.01);与Emp组治疗后比较,Lir、Aca组治疗后SUA、HDL-C升高,LDL-C降低(P0.01)。结论利拉鲁肽治疗超重/肥胖的T2DM患者换用恩格列净后,除SUA及HDL-C降低、LDL-C升高外,其降糖、减重、降压的效果与继续原药治疗相同。     

利拉鲁肽对2型糖尿病合并冠心病病人血清免疫因子水平的影响

目的探讨利拉鲁肽对2型糖尿病合并冠心病病人血清免疫因子水平的影响。方法将2017年3月—2018年2月收治的2型糖尿病合并冠心病病人92例随机分为对照组与利拉鲁肽组,各46例。对照组给予常规综合治疗,利拉鲁肽组在上述治疗基础上每日早餐前皮下注射利拉鲁肽注射液,两组均持续治疗12周。检测并比较超敏C反应蛋白(hs-CRP)、肿瘤坏死因子-α(TNF-α)、白介素-6(IL-6)、空腹血糖(FPG)、餐后2 h血糖(2 hPG)、糖化血红蛋白(HbA1c)、左室射血分数(LVEF)、舒张早期最大峰值速度(E峰)、舒张晚期最大峰值速度(A峰)、E/A比值及两组临床疗效。结果治疗后,两组血清hs-CRP、TNF-α、IL-6水平降低(P0.01),FPG、2 hPG、HbA1c水平降低(P0.01),LVEF、E峰、E/A比值升高(P0.05),A峰降低(P0.05);与对照组比较,利拉鲁肽组血清hs-CRP、TNF-α、IL-6水平降低(P0.01),FPG、2 hPG、HbA1c水平降低(P0.01),LVEF、E峰、E/A比值升高(P0.05),A峰降低(P0.05)。利拉鲁肽组有效率高于对照组(95.65%与78.26%,P0.05)。结论利拉鲁肽能改善2型糖尿病合并冠心病病人免疫因子、血糖及心功能等指标。     

利拉鲁肽对高脂饲养大鼠骨骼肌脂质沉积及骨骼肌超微结构的影响

目的研究胰高血糖素样肽1类似物利拉鲁肽对高脂喂养胰岛素抵抗(IR)大鼠骨骼肌脂质沉积及骨骼肌细胞超微结构的影响。方法雄性Wistar大鼠54只,随机普通饲养16只、高脂饲养38只,饲养8周后,各取5只大鼠判定大鼠IR状态,造模成功后,将高脂饲养大鼠分为高脂组、干预组1[利拉鲁肽100μg/(kg·d)]、干预组2[利拉鲁肽200μg/(kg·d)],每组11只,另11只普通饲养为对照组。药物干预2周后,检测骨骼肌内甘油三酯(mTG)、长链脂肪酰辅酶A(LCACoA),透射电镜观察大鼠骨骼肌细胞超微结构改变。结果与对照组比较,高脂组mTG、LCACoA含量升高[(19.58±1.63)μmol/g vs(9.99±0.90)μmol/g;(6.70±0.18)nmol/g vs(2.51±0.18)nmol/g,P0.01];与高脂组比较,干预组1LCACoA含量下降[(6.10±0.37)nmol/g vs(6.70±0.18)nmol/g,P0.05],干预组2mTG、LCACoA含量明显下降[(13.57±0.66)nmol/g vs(19.58±1.63)nmol/g,(4.73±0.31)nmol/g vs(6.70±0.18)nmol/g,P0.01]。干预组1和干预组2较高脂组和对照组脂滴减少、线粒体肿胀减轻。结论利拉鲁肽可呈浓度依赖性减少高脂喂养大鼠mTG和LCACoA含量,可能是减轻IR的原因之一。     

利拉鲁肽经AMPK途径对平滑肌细胞KCa3.1蛋白表达的影响

目的探讨利拉鲁肽经激活腺苷酸活化的蛋白激酶(AMPK)途径对平滑肌细胞KCa3.1蛋白表达的影响。方法制备SD大鼠血管平滑肌细胞模型,大鼠主动脉平滑肌细胞采用利拉鲁肽进行干预,测定未加入利拉鲁肽及加入利拉鲁肽15 min后磷酸化AMPK(PAMPK)/AMPK比值。将平滑肌细胞分为4组培养:A组为正常组,B组采用血管紧张素Ⅱ100 nmol/L,C组采用利拉鲁肽1μmol/L+血管紧张素Ⅱ100 nmol/L,D组采用利拉鲁肽1μmol/L+AMPK阻滞剂4μmol/L+血管紧张素Ⅱ100 nmol/L。培养72 h后使用Western-Blotting检测KCa3.1蛋白表达。结果显微镜下可见细胞呈长梭状、三角状,α-actin细胞免疫荧光染色后,胞浆着色为红色,确认为血管平滑肌细胞。利拉鲁肽与大鼠血管平滑肌作用15 min后,与基线比较PAMPK水平明显上升,PAMPK与AMPK比值明显上调,差异有统计学意义(P0.05)。C组平滑肌细胞KCa3.1蛋白表达较B组下降(P0.05)。结论利拉鲁肽可激活AMPK细胞通路,抑制平滑肌细胞上KCa3.1蛋白表达。     

利拉鲁肽通过调节SIRT1改善高糖诱导的大鼠H9c2细胞氧化应激损伤

目的探究利拉鲁肽(liraglutide, LRG)对高糖诱导的心肌细胞(H9c2)氧化应激损伤的影响及其潜在机制。方法采用高糖处理H9c2细胞24 h建立心肌细胞体外损伤模型, 给予不同浓度利拉鲁肽(10、100、1 000 nmol/L)干预, 用CCK-8检测细胞活力, 倒置显微镜观察细胞形态结构的改变。利拉鲁肽(100 nmol/L)干预高糖处理H9c2细胞24 h后检测细胞上清液中乳酸脱氢酶(LDH)、超氧化物歧化酶(SOD)和丙二醛含量;RT-PCR和Western印迹法检测沉默信息调节因子1(SIRT1)和叉头转录因子1(FOXO1)mRNA及蛋白水平;Western印迹法检测FOXO1蛋白乙酰化水平;应用小干扰RNA(siRNA)技术沉默SIRT1的H9c2细胞株验证SIRT1在其中的作用。结果与对照组相比, 高糖组细胞活力降低, 细胞结构受损, 细胞上清液中LDH、丙二醛含量显著升高, SOD含量降低, 氧化应激加重, SIRT1表达降低, FOXO1乙酰化水平升高(均P<0.05);与高糖组比较, 给予利拉鲁肽干预后细胞活力升高, 心肌细胞结构形态和氧化应激水...     

利拉鲁肽对小鼠骨骼肌细胞葡萄糖转运子4转位的作用

目的 探讨胰高血糖素样肽1 （GLP-1）类似物利拉鲁肽对小鼠骨骼肌细胞葡萄糖转运子4（GLUT4）转位的作用及可能机制.方法 在过表达带有HA表位GLUT4的小鼠骨骼肌细胞株C2C12（C2C12-GLUT4H）,分为正常对照组、胰岛素组（100 nmol/L）、利拉鲁肽1组（100 nmol/L）、利拉鲁肽2组（1 000 nmol/L）、5-氨基咪唑-4-甲酰1-β-D呋喃糖苷（AICAR）（腺苷酸活化蛋白激酶激动剂）组（2 mmol/L）.通过ELISA法测定细胞膜上C2C12-GLUT4HA,检测各组对C2C12-GLUT4HA细胞GLUT4转位的作用.应用Western blotting检测介导GLUT4转位的信号分子蛋白激酶B（AKT）、腺苷酸活化蛋白激酶（AMPK）磷酸化水平以及GLUT4蛋白表达水平.采用Student＇s t检验或单因素方差分析进行统计分析.结果 利拉鲁肽组的GLUT4转位较对照组相比明显上升[分别是对照组的（1.53±0.28）倍、（1.41±0.41）倍,F=13.4798,P＜0.05];利拉鲁肽刺激组与对照组相比能够使pAMPK水平升高[分别是对照组的（1.79±0.31）倍、（1.54±0.18）倍,F=20.0999,P＜0.05],而对pAKT无明显影响（P＞0.05）.结论 利拉鲁肽可通过激活AMPK从而促进小鼠骨骼肌细胞GLUT4转位的增加.     

Aggregation Fails to Increase Cytosolic [Ca(2+)] in Aequorin-loaded Human Platelets

Studies were performed to determine whether formation of platelet aggregates itself, could cause an increase in cytosolic [Ca(2+)]([Ca(2+)](i)) which is independent of that resulting from the addition of agonists which induce aggregation. An increase in [Ca(2+)](i) did not coincide with aggregate formation when this response was dissociated from the addition of ADP or thrombin by delay either in initiating stirring or, for ADP, in adding fibrinogen. No increase in [Ca(2+)](i) occurred when aggregation was induced by addition of 1,2-dioctanoylglycerol or of ristocetin, or for chymotrypsin-treated platelets by addition of fibrinogen. The results demonstrate clearly that aggregate formation does not cause an increase in [Ca(2+)](i), and therefore exclude this possibility as an explanation for the discrepancies observed when [Ca(2+)](i) is measured, using aequorin and Fura2 as probes and as an underlying mechanism to account for contact-induced responses.     

Na(+)-Ca(2+) exchange current and submembrane [Ca(2+)] during the cardiac action potential

Na(+)-Ca(2+) exchange (NCX) is crucial in the regulation of [Ca(2+)](i) and cardiac contractility, but key details of its dynamic function during the heartbeat are not known. In the present study, we assess how NCX current (I(NCX)) varies during a rabbit ventricular action potential (AP). First, we measured the steady-state voltage and [Ca(2+)](i) dependence of I(NCX) under conditions when [Ca(2+)](i) was heavily buffered. We then used this relationship to infer the submembrane [Ca(2+)](i) ([Ca(2+)](sm)) sensed by NCX during a normal AP and [Ca(2+)](i) transient (when the AP was interrupted to produce an I(NCX) tail current). The [Ca(2+)](i) dependence of I(NCX) at -90 mV allowed us to convert the peak inward I(NCX) tail currents to [Ca(2+)](sm). Peak [Ca(2+)](sm) measured via this technique was >3.2 micromol/L within < 32 ms of the AP upstroke (versus peak [Ca(2+)](i) of 1.1 micromol/L at 81 ms measured with the global Ca(2+) indicator indo-1). The voltage and [Ca(2+)](sm) dependence of I(NCX) allowed us to infer I(NCX) during the normal AP and Ca(2+) transient. The early rise in [Ca(2+)](sm) causes I(NCX) to be inward for the majority of the AP. Thus, little Ca(2+) influx via NCX is expected under physiological conditions, but this can differ among species and in pathophysiological conditions.     

血清钙离子浓度对DAVNP伴AVNRT电生理特性的影响

本文观察了应用葡萄糖酸钙静脉注射提高血清[Ca~(2+)]后,对房室结双径路(DAVNP)伴房室结折返性心动过速(AVNRT)的影响.结果示血清钙离子浓度从1.13±0.15mmol/L提高到1.32±0.13mmol/L,(P<0.02).使快径路有效不应期从365±45ms延长到400±35ms,P<0.01,有极显著差异.对慢径路不应期和快、慢径路传导速度均无明显影响.使传导曲线“中断”表现更明显,对AVNRT折返窗有显著增宽作用,P<0.01,使AVNRT更易诱发.同时观察了血清[Ca~(2+)]升高对正常房室结的影响,发现血清[Ca~(2+)]升高时,慢径路电生理特性与房室结相似,受影响不明显,而快径路有效不应期明显延长,与房室结电生理特性有明显区别.本文认为通过提高血清[Ca~(2+)]的方法对提高房室结双径路的诊断准确率具有较高价值.     

高血压病患者血小板Na~ -H~ 交换与Ca~(2 )内流、Ca~(2 )结合力的关系

细胞内pH对血管平滑肌结构和功能有重要影响,本文通过观察高血压病患者血小板Na~ -H~ 交换活性、血小板Ca~(2 )内流和Ca~(2 )结合力等指标,探讨了细胞Na~ -H~ 交换活性和Ca~(2 )代谢与血压间的关系。     

氯通道参与脑血管平滑肌细胞Ca2+池操纵性Ca2+内流

研究Cl-通道在牛脑血管平滑肌细胞Ca2+池操纵性Ca2+内流中的作用.采用培养的脑血管平滑肌细胞,在生物荧光双波长影像分析系统用Fura-2/Am荧光探针测定单个细胞内游离Ca2+浓度.结果发现① Cl-通道阻断剂DIDS(0.75 μmol/L)能降低内皮素1(10-7 mol/L)刺激引起的脑血管平滑肌细胞Ca2+内流,抑制率为29.6%±3.9%,随后加入Cl-通道阻断剂NPPB(10 μmol/L)能继续降低平台相,抑制率为44.9%±8.7%;交换加药顺序,NPPB能降低内皮素1刺激引起的Ca2+内流,DIDS能进一步降低Ca2+内流.②DIDS(0.75 μmol/L)能降低三磷酸腺苷(10 μmol/L)刺激引起的脑血管平滑肌细胞Ca2+内流,抑制率为26.7%±10.5%,随后加入NPPB(10 μmol/L)能继续降低平台相,抑制率为54.3%±9.6%;交换加药顺序,NPPB能降低三磷酸腺苷刺激引起的Ca2+内流,DIDS能进一步降低Ca2+内流.③DIDS(0.75 μmol/L)能降低环匹阿尼酸(10 μmol/L)刺激引起的脑血管平滑肌细胞Ca2+内流,抑制率为26.5%±5.0%,随后加入NPPB(10 μmol/L)能继续降低平台相,抑制率为46.1%±4.2%;交换加药顺序,NPPB能降低环匹阿尼酸刺激引起的Ca2+内流,DIDS能进一步降低Ca2+内流.提示对DIDS、NPPB敏感的非同一性Cl-通道参与内皮素1、三磷酸腺苷、环匹阿尼酸触发的脑血管平滑肌细胞 Ca2+池操纵性Ca2+内流.     

24例老年肺心病患者红细胞钙－ATP酶和钙镁含量的变化

目的观察老年肺心病患者红细胞膜钙－ＡＴＰ酶（钙泵）活性和红细胞内Ｃａ２、Ｍｇ２＋含量的变化，初步探讨其发生机制及意义。方法采用生化方法和原子吸收法测定上述指标，并与非老年肺心病患者及老年健康者比较。结果老年肺心病组（２４例）红细胞钙泵活性（μｍｏｌｐｉ·ｍｇ－１／ｈ）、Ｃａ２＋含量（μｍｏｌ／ｇ）、Ｍｇ２＋含量（μｍｏｌ／ｇ）分别为０．２３±０．１０、７．４６±１．８２、８．２１±０．８４；非老年肺心病组（２０例）分别为０．３２±０．１１、６．０１±１．５２、８．７４±０．７２；老年健康组（１２名）分别为０．４２±０．１５、４．５１±１．４４、９．０２±１．０８。老年肺心病组与后两组比较，红细胞钙泵活性及Ｍｇ２＋含量降低，Ｃａ２＋含量增高（Ｐ值＜０．０５、０．０１或０．００１）；在肺心病伴呼吸衰竭和心力衰竭时上述异常改变更为明显。结论红细胞膜钙泵活性降低及其细胞内Ｃａ２＋、Ｍｇ２＋含量异常变化，在老年人肺心病的发病中可能具有重要作用     

Ca~(2 )预处理和缺血预处理对大鼠心脏Ca~(2 )反常损伤的影响

给离体大鼠心脏进行5次1分钟无Ca~(2 )继5分钟复Ca~(2-)灌流预处理后,可使随后Ca~(2-)反常损伤明显减轻,表现为心肌细胞蛋白质丢失量减少,冠状动脉痉挛减轻.本研究进一步应用2次10分钟缺血,继10分钟再灌注进行缺血预处理,结果显示这一方案未能减轻Ca~(2 )反常所致心肌损伤.如在Ca~(2-)预处理过程中给予腺苷A_1受体阻滞剂8-SPT,可以阻断Ca~(2 )预处理的保护作用,提示腺苷A_1受体兴奋可能是这一保护机制的重要环节.     

Activation of connexin-43 hemichannels can elevate [Ca(2+)]i and [Na(+)]i in rabbit ventricular myocytes during metabolic inhibition.

ATP depletion due to ischemia or metabolic inhibition (MI) causes Na(+) and Ca(2+) accumulation in myocytes, which may be in part due to opening of connexin-43 hemichannels. Halothane (H) has been shown to reduce conductance of connexin-43 hemichannels and to protect the heart against ischemic injury. We therefore investigated the effect of halothane on [Ca(2+)]i and [Na(+)]i in myocytes during MI. Isolated rabbit left ventricular myocytes were loaded with 4 microM fluo-3 AM for 30 min, or with 5 microM sodium green AM for 60 min at 37 degrees C. After washing, the myocytes were exposed to: (1) Normal HEPES solution; (2) MI solution (2 mM NaCN, 20 mM 2-deoxy-D-glucose and 0-glucose); or (3) MI+H (0.95 mM, 4.7 mM) for 60 min. Propidium iodide (PI, 25 microM) was added to all samples before data acquisition. The fluorescence intensity was measured by flow cytometry with 488 nm excitation and 530 nm emission for fluo-3 or sodium green, and 670 nm for PI. The [Ca(2+)]i and [Na(+)]i were then calculated by calibration. In some experiments, the effect of 10 microM tetrodotoxin (TTX) and 20 microM nifedipine (NIF) were studied. Metabolic inhibition for 60 min caused a significant increase in [Ca(2+)]i and [Na(+)]i in myocytes when compared to controls, which was significantly reduced by halothane in a dose-dependent fashion. In the presence of TTX and NIF, halothane also significantly reduced the rise in the [Ca(2+)]i and [Na(+)]i in myocytes subjected to MI. 1-heptanol, another gap junction blocker, had similar effects. Thus, halothane reduced [Ca(2+)]i and [Na(+)]i overload produced by MI in myocytes. This effect is not solely due to block of voltage-gated Na(+) and Ca(2+) channels, and is likely mediated by inhibiting the opening of connexin-43 hemichannels.     

Chronic hypoxia increases intracellular Ca~(2+) concentration and augments proliferation by enhancing store-operated Ca~(2+) entry in pulmonary arterial smooth muscle cells

<正>Objective To determine whether store-operated Ca~(2+) entry(SOCE)is involved in chronic hypoxia-induced alteration of intracellular Ca~(2+)concentration ([Ca~(2+)]_i)and proliferation in pulmonary arterial smooth muscle cells(PASMC).Methods Rat PASMCs were cultured and treated in normoxia(21%O_2)or hypoxia(4%O_2)condition.The proliferation of PASMC     

SJAMP对血小板胞内游离钙水平的影响

目的：探讨Ca2 在SJAMP诱导血小板聚集中的作用。方法：以Fura-2为钙荧光探针，应用双波长法测定了SJAMP对血小板胞内游离钙水平的影响。结果：发现SJAMP在100μg／ml时对血小板胞浆游离钙的影响最为显著，可使正常人血小板胞内钙水平从71．30±7.66nmol／L升至93．96±10．24nmol/L（n＝10），在胞外存在1mmol／LCa2 时，SJAMP引起胞内游离钙升高幅度更大．可达116．72±10．66nmol／L（n=10）。另一方面，SJAMP对血小板胞内游离钙的影响，与其它诱导剂相比，其升高幅度较小且时限较长，同时如果血小板预先与环氧化酶抑制剂孵育．则SJAMP对血小板胞内钙的升高作用明显受抑。结论：推测SJAMP对血小板胞内钙的影响可能是一花生四烯酸及其代谢物有关的过程。