1.上海中医药大学(上海 201203)
2.上海中医药大学附属上海市中西医结合医院脉管病科(上海 200082)
3.上海中医药大学附属岳阳中西医结合医院神经内科(上海 200437)
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张永康,刘家睿,殷康力等.银杏二萜内酯葡胺注射液对急性缺血性脑卒中患者血清半乳糖凝集素⁃3水平的影响[J].上海中医药大学学报,2023,37(01):31-37.
ZHANG Yongkang,LIU Jiarui,YIN Kangli,et al.Effect of Ginkgo diterpenoid lactone glucosamine injection on serum galectin⁃3 level in patients with acute ischemic stroke[J].Academic Journal of Shanghai University of Traditional Chinese Medicine,2023,37(01):31-37.
张永康,刘家睿,殷康力等.银杏二萜内酯葡胺注射液对急性缺血性脑卒中患者血清半乳糖凝集素⁃3水平的影响[J].上海中医药大学学报,2023,37(01):31-37. DOI: 10.16306/j.1008-861x.2023.01.005.
ZHANG Yongkang,LIU Jiarui,YIN Kangli,et al.Effect of Ginkgo diterpenoid lactone glucosamine injection on serum galectin⁃3 level in patients with acute ischemic stroke[J].Academic Journal of Shanghai University of Traditional Chinese Medicine,2023,37(01):31-37. DOI: 10.16306/j.1008-861x.2023.01.005.
目的,2,探讨银杏二萜内酯葡胺注射液对急性缺血性脑卒中(AIS)患者血清半乳糖凝集素-3(gal-3)水平的影响,并观察血清gal-3水平变化与患者神经功能缺损症状和预后的关系。,方法,2,纳入88例AIS患者,随机分为对照组和试验组,每组各44例。两组患者均给予阿司匹林肠溶片口服,在此基础上,试验组患者给予银杏二萜内酯葡胺注射液静脉滴注,对照组患者给予安慰剂注射液静脉滴注,治疗周期为14 d。于治疗前后检测并比较两组患者的血清gal-3、白介素-1β(IL-1β)、IL-6、肿瘤坏死因子-α(TNF-α)水平;于治疗前及治疗第14、28、90天,评估并比较两组患者的美国国立卫生研究院卒中量表(NIHSS)评分;于治疗前及治疗第90天,评估并比较两组患者的改良Rankin量表(mRS)评分。对患者的血清gal-3、IL-1β、IL-6、TNF-α水平变化与患者预后不良(治疗第90天的mRS评分≥3分)之间的相关性进行分析。,结果,2,研究过程中,对照组剔除或脱落8例患者,试验组剔除或脱落8例患者,最终纳入统计分析者对照组36例、试验组36例。①治疗第14、28、90天,两组患者的NIHSS评分较治疗前均明显降低(,P<,0.05),且试验组患者的评分低于对照组(,P<,0.05)。②治疗第90天,两组患者的mRS评分较治疗前均明显降低(,P,<,0.05),且试验组患者的评分低于对照组(,P,<,0.05)。③治疗后,试验组患者的血清gal-3水平较治疗前明显降低(,P,<,0.05),对照组患者的血清gal-3水平较治疗前明显升高(,P,<,0.05),且试验组患者的血清gal-3水平显著低于对照组(,P,<,0.05)。④治疗后,试验组患者的血清IL-1β水平较治疗前明显降低(,P,<,0.05),TNF-α水平明显升高(,P,<,0.05)。⑤预后不良与血清gal-3、IL-1β水平升高呈正相关关系(,P,<,0.05),预后不良与血清TNF-α水平升高呈负相关关系(,P,<,0.05)。,结论,2,银杏二萜内酯葡胺注射液可有效改善AIS患者的神经功能缺损症状及预后,其机制可能与降低患者的血清gal-3水平进而达到神经保护作用相关。
Objective: To explore the influence of Ginkgo diterpenoid lactone glucosamine injection on the level of serum galectin-3 (gal-3) in patients with acute ischemic stroke (AIS), and observe the relationship between the changes of serum gal-3 level and the neurological deficit symptoms and prognosis of the patients.,Methods,2,A total of 88 patients with AIS were enrolled and randomly divided into the control group and trial group, 44 cases in each group. The patients in both groups were orally treated with aspirin enteric-coated tablets. Based on above, the patients in the trial group were treated with intravenous drip of Ginkgo diterpenoid lactone glucosamine injection, and the patients in the control group were treated with intravenous drip of placebo injection. The treatment course was 14 d. Before and after treatment, the levels of serum gal-3, interleukin-1β (IL-1β), IL-6 and tumor necrosis factor-α (TNF-α) in the two groups were detected and compared. Before treatment and on the 14th, 28th and 90th day of treatment, the scores of National Institutes of Health Stroke Scale (NIHSS) in the two groups were evaluated and compared. Before treatment and on the 90th day of treatment, the scores of modified Rankin Scale (mRS) in the two groups were evaluated and compared. The correlation between the changes of serum gal-3, IL-1β, IL-6 and TNF-α levels and the poor prognosis (mRS scores≥3 points on the 90th day of treatment) was analyzed.,Results,2,During the study, 8 patients in the control group were excluded or dropped out, and 8 patients in the trial group were excluded or dropped out. Finally, 36 cases in the control group and 36 cases in the trial group were included in the statistical analysis. ①On the 14th, 28th and 90th,day of treatment, the scores of NIHSS in the two groups were significantly decreased compared with those before treatment (,P,<,0.05), and the score of the trial group was lower than that of the control group (,P,<,0.05). ②On the 90th day of treatment, the scores of mRS in the two groups were significantly decreased compared with those before treatment (,P,<,0.05), and the score of the trial group was lower than that of the control group (,P,<,0.05). ③After treatment, the serum gal-3 level of the trial group was significantly decreased compared with that before treatment (,P,<,0.05), the serum gal-3 level of the control group was significantly increased compared with that before treatment (,P,<,0.05), and the serum gal-3 level of the trial group was significantly lower than that of the control group (,P,<,0.05). ④After treatment, the serum IL-1β level of the trial group was significantly decreased compared with that before treatment (,P,<,0.05), and the TNF-α level was significantly increased (,P,<,0.05). ⑤Poor prognosis was positively correlated with the increased serum gal-3 and IL-1β levels (,P,<,0.05), and poor prognosis was negatively correlated with the increased serum TNF-α level (,P,<,0.05).,Conclusion,2,Ginkgo diterpenoid lactone glucosamine injection can effectively improve the symptoms and prognosis of neurological deficits in patients with AIS, and its mechanism may be related to the reduction of the serum gal-3 level in patients to achieve neuroprotection.
急性缺血性脑卒中银杏二萜内酯半乳糖凝集素-3
acute ischemic strokeGingko diterpene lactonegalectin-3
WANG W, JIANG B, SUN H, et al. Prevalence, Incidence, and Mortality of Stroke in China: Results from a Nationwide Population-Based Survey of 480 687 Adults[J]. Circulation, 2017, 135(8): 759-771.
CHAMORRO Á, DIRNAGL U, URRA X, et al. Neuroprotection in acute stroke: targeting excitotoxicity, oxidative and nitrosative stress, and inflammation[J]. Lancet Neurol, 2016, 15(8): 869-881.
ESENWA C C, ELKIND M S. Inflammatory risk factors, biomarkers and associated therapy in ischemic stroke[J]. Nat Rev Neurol, 2016, 12(10): 594-604.
华玉凡. 银杏二萜内酯葡胺注射液治疗缺血性卒中恢复期(痰瘀阻络证)的临床研究[D]. 武汉: 湖北中医药大学, 2015: 42.
HUA Y F. Clinical Observation on Diterpene Ginkgolides Meglumine Injection for Syndrome of Stagnant Phlegm Blocking Collaterals in Convalescence of Ischemia Stroke[D]. Wuhan: Hubei University of Chinese Medicine, 2015: 42.
FANG W, SHA L, KODITHUWAKKU N D, et al. Attenuated blood-brain barrier dysfunction by XQ-1H following ischemic stroke in Hyperlipidemic rats[J]. Mol Neurobiol, 2015, 52(1): 162-175.
FANG W, DENG Y, LI Y, et al. Blood brain barrier permeability and therapeutic time window of Ginkgolide B in ischemia-reperfusion injury[J]. Eur J Pharm Sci, 2010, 39(1-3): 8-14.
LI S Q, ZHANG Y, YANG L J. Improving effect of Ginkgolide B on mitochondrial respiration of ischemic neuron after cerebral thrombosis in tree shrewa[J]. Chin Med J (Engl), 2007, 120(17): 1529-1533.
GILL I, KAUR S, KAUR N, et al. Phytochemical Ginkgolide B attenuates amyloid-β1-42 induced oxidative damage and altered cellular responses in human neuroblastoma SH-SY5Y cells[J]. J Alzheimers Dis, 2017, 60(S1): S25-S40.
CHEN M, ZOU W, CHEN M, et al. Ginkgolide K promotes angiogenesis in a middle cerebral artery occlusion mouse model via activating JAK2/STAT3 pathway[J]. Eur J Pharmacol, 2018, 833: 221-229.
WU X, ZHOU C, DU F, et al. Ginkgolide B preconditioning on astrocytes promotes neuronal survival in ischemic injury via up-regulating erythropoietin secretion[J]. Neurochem Int, 2013, 62(2): 157-164.
ROTSHENKER S. The role of Galectin-3/MAC-2 in the activation of the innate-immune function of phagocytosis in microglia in injury and disease[J]. J Mol Neurosci, 2009, 39(1-2): 99-103.
WANG A, ZHONG C, ZHU Z, et al. Serum Galectin-3 and Poor Outcomes Among Patients with Acute Ischemic Stroke[J]. Stroke, 2018, 49(1): 211-214.
中华医学会神经病学分会, 中华医学会神经病学分会脑血管病学组. 中国急性缺血性脑卒中诊治指南2018[J]. 中华神经科杂志, 2018, 51(9): 666-682.
Neurology Society of Chinese Medical Association, Cerebrovascular Disease Group of Neurology Society of Chinese Medical Association. Chinese guidelines for diagnosis and treatment of acute ischemic stroke 2018[J]. Chinese Journal of Neurology, 2018, 51(9): 666-682.
王欢, 魏书艳, 杨凡, 等. 丹参多酚酸对老年脑卒中患者血清半乳糖凝集素-3、超敏C反应蛋白水平的影响[J]. 中国现代医学杂志, 2019, 29(17): 75-78.
WANG H, WEI S Y, YANG F, et al. Effect of Salvianolate injection on plasma Galectin-3 and C-reactive protein in elderly patients with stroke[J]. China Journal of Modern Medicine, 2019, 29(17): 75-78.
BOUTIN H, LEFEUVRE R A, HORAI R, et al. Role of IL-1alpha and IL-1beta in ischemic brain damage[J]. J Neurosci, 2001, 21(15): 5528-5534.
YOSHIMOTO T, HOUKIN K, TADA M, et al. Induction of cytokines, chemokines and adhesion molecule mRNA in a rat forebrain reperfusion model[J]. Acta Neuropathol, 1997, 93(2):154-158.
BUTTINI M, SAUTER A, BODDEKE H W. Induction of interleukin-1 beta mRNA after focal cerebral ischaemia in the rat[J]. Brain Res Mol Brain Res, 1994, 23(1-2): 126-134.
HURN P D, SUBRAMANIAN S, PARKER S M, et al. T- and B-cell-deficient mice with experimental stroke have reduced lesion size and inflammation[J]. J Cereb Blood Flow Metab, 2007, 27(11): 1798-1805.
DAVIES C A, LODDICK S A, TOULMOND S, et al. The progression and topographic distribution of interleukin-1beta expression after permanent middle cerebral artery occlusion in the rat[J]. J Cereb Blood Flow Metab, 1999, 19(1): 87-98.
YAMASAKI Y, MATSUURA N, SHOZUHARA H, et al. Interleukin-1 as a pathogenetic mediator of ischemic brain damage in rats[J]. Stroke, 1995, 26(4): 676-680.
CLARK W M, RINKER L G, LESSOV N S, et al. Lack of interleukin-6 expression is not protective against focal central nervous system ischemia[J]. Stroke, 2000, 31(7):1715-1720.
YAMASHITA T, SAWAMOTO K, SUZUKI S, et al. Blockade of interleukin-6 signaling aggravates ischemic cerebral damage in mice: possible involvement of Stat3 activation in the protection of neurons[J]. J Neurochem, 2005, 94(2): 459-468.
HERRMANN O, TARABIN V, SUZUKI S, et al. Regulation of body temperature and neuroprotection by endogenous interleukin-6 in cerebral ischemia[J]. J Cereb Blood Flow Metab, 2003, 23(4): 406-415.
SMITH C J, EMSLEY H C, GAVIN C M, et al. Peak plasma interleukin-6 and other peripheral markers of inflammation in the first week of ischaemic stroke correlate with brain infarct volume, stroke severity and long-term outcome[J]. BMC Neurol, 2004, 4: 2.
RALLIDIS L S, VIKELIS M, PANAGIOTAKOS D B, et al. Inflammatory markers and in-hospital mortality in acute ischaemic stroke[J]. Atherosclerosis, 2006, 189(1): 193-197.
HALLENBECK J M. The many faces of tumor necrosis factor in stroke[J]. Nat Med, 2002, 8(12): 1363-1368.
PAN W, KASTIN A J. Tumor necrosis factor and stroke: role of the blood-brain barrier[J]. Prog Neurobiol, 2007, 83(6): 363-374.
YANG G Y, GONG C, QIN Z, et al. Inhibition of TNFalpha attenuates infarct volume and ICAM-1 expression in ischemic mouse brain[J]. Neuroreport, 1998, 9(9): 2131-2134.
BARONE F C, ARVIN B, WHITE R F, et al. Tumor necrosis factor-alpha. A mediator of focal ischemic brain injury[J]. Stroke, 1997, 28(6): 1233-1244.
GINIS I, JAISWAL R, KLIMANIS D, et al. TNF-alpha-induced tolerance to ischemic injury involves differential control of NF-kappaB transactivation: the role of NF-kappaB association with p300 adaptor[J]. J Cereb Blood Flow Metab, 2002, 22(2): 142-152.
BRUCE A J, BOLING W, KINDY M S, et al. Altered neuronal and microglial responses to excitotoxic and ischemic brain injury in mice lacking TNF receptors[J]. Nat Med, 1996, 2(7): 788-794.
AMANTEA D, NAPPI G, BERNARDI G, et al. Post-ischemic brain damage: pathophysiology and role of inflammatory mediators[J]. FEBS J, 2009, 276(1): 13-26.
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