المؤلفون: YUAN Jing, CHENG Yangyang, LI Hongmei, ZHOU Keji

المصدر: Chinese Journal of Immunology; Jan2024, Vol. 40 Issue 2, p247-251, 5p

مصطلحات موضوعية: ENDOTHELIAL cells, GLUTATHIONE peroxidase, MEMBRANE potential, LACTATE dehydrogenase, MITOCHONDRIAL membranes, NLRP3 protein, ADIPONECTIN

مستخلص: Objective: To investigate effects of adiponectin on survival, oxidative stress, inflammation and mitochondrial function of endothelial cell HUVEC induced by high glucose, and its potential mechanism. Methods: HUVEC cells were cultured with 5, 25 mmol/L glucose and divided into normal (NC) group and high glucose (HG) group. Adiponectin (1, 2, 4 µg/ml) treatment of high glucose induced endothelial cells were divided into low dose (L), medium dose (M) and high dose (H) groups. HUVEC cells treated with PBS, LPS and 4 µg/ml adiponectin were labeled as H+PBS group and H+LPS group. CCK8 and Annexin V-FITC/PI double staining were used to detect cell proliferation and apoptosis. Western blot was used to detect protein expressions of Cleaved caspase-3, NLPR3, amino acid transporter (ASC), Caspase-1, p-nuclear factor κB inhibitor protein (p-I-κBα) . ELISA was used to detect concentrations of lactate dehydrogenase (LDH), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), malondialdehyde (MDA), IL-4, IL-6 and IL-1β. ROS fluorescence activity was detected by immunofluorescence. Mitochondrial membrane potential was detected by JC-1 staining. NLRP3 expression was detected by RT-qPCR. Results: Compared with NC group, 48 h, 72 h and 96 h survival rates of endothelial cells were significantly reduced, apoptosis rate was significantly increased, and levels of LDH, SOD, MDA, mitochondrial membrane potential, IL-4, IL-6 and IL-1β in cell supernatant were significantly increased, concentrations of ROS and GSH-Px were significantly decreased, and protein expressions of Cleared caspase-3, NLRP3, Caspase-1 and p-NF-κB were significantly increased, p-I-κBα expression was decreased significantly (P<0.05) . Adiponectin inhibited above changes of endothelial cells induced by high glucose in a concentration dependent manner. LPS attenuated above protective effects of adiponectin on HG induced endothelial cells. Conclusion: Adiponectin can reduce survival inhibition, oxidative stress, inflammatory response and mitochondrial dysfunction of endothelial cells induced by high glucose, whose protecting mechanism may be related to NF-κB pathway. [ABSTRACT FROM AUTHOR]

: Copyright of Chinese Journal of Immunology is the property of Medical Periodical Society of Jilin and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

العنوان البديل: Effects of ligustrazine on inflammation and oxidative stress in rat cardiomyocytes induced by lipopolysaccharide. (English)

المؤلفون: 孙芳园, 孟佳磊, 马宇慧, 耿 欢, 张 涛

المصدر: Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu; 7/18/2023, Vol. 27 Issue 20, p3253-3258, 6p

مصطلحات موضوعية: TUMOR necrosis factors, REACTIVE oxygen species, LACTATE dehydrogenase, PROPIDIUM iodide, INTERLEUKIN-1 receptors, OXIDATIVE stress, MYELOID differentiation factor 88

الملخص (بالإنجليزية): BACKGROUND: Sepsis-induced myocardial injury is related to inflammatory response and oxidative stress injury. Previous studies have shown that ligustrazine has many functions such as anti-oxidation and maintaining calcium homeostasis. OBJECTIVE: To investigate the effects of ligustrazine on inflammation and oxidative stress in lipopolysaccharide-induced rat cardiomyocytes. METHODS: Rat cardiomyocytes were induced by lipopolysaccharide (1 μg/mL) to establish septic cardiomyocyte inflammatory models. Twenty-four hours after intervention with different concentrations of ligustrazine (40, 80, 160 μmol/L), the samples were collected and detected. The effects of ligustrazine on the release of lactate dehydrogenase and reactive oxygen species from H9C2 cells induced by lipopolysaccharide were detected. Apoptosis was observed by fluorescence microscope. RT-qPCR was used to detect the changes of inflammatory factors such as interleukin-1 β, tumor necrosis factor-α, and interleukin-6 as well as the expression of Toll like receptor 4 and MyD88. RESULTS AND CONCLUSION: Compared with the normal control group, the expression of lactate dehydrogenase and reactive oxygen species in H9C2 cells increased significantly in the model group (P < 0.05) and a large number of cells were stained with propidium iodide under fluorescence microscope. The expression levels of interleukin-1β, tumor necrosis factor-α, and interleukin-6 were significantly increased (P < 0.05) and the expression of Toll like receptor 4 and MyD88 genes were significantly increased in the model group compared with the normal control group (P < 0.05). Compared with the model group, ligustrazine treatment could effectively inhibit the release of lactate dehydrogenase and reactive oxygen species, reduce the number of H9C2 cells stained by propidium iodide, downregulate the expression of interleukin-1β, tumor necrosis factor α and interleukin-6, and suppress the expression of Toll like receptor 4 and MyD88 genes (P < 0.05). To conclude, ligustrazine may reduce intracellular inflammatory factors and oxidative stress by inhibiting the expression of Toll like receptor 4/MyD88. [ABSTRACT FROM AUTHOR]

Abstract (Chinese): 背景：脓毒症心肌损伤与炎症反应及氧化应激损伤有关。既往研究表明川芎嗪具有抗氧化、维持钙稳态等多种功能。 目的：探讨川芎嗪对脂多糖诱导的大鼠心肌细胞炎症反应及氧化应激作用的影响。 方法：利用脂多糖(1 μg/mL)诱导大鼠心肌细胞建立脓毒症心肌细胞炎性模型，通过不同浓度的川芎嗪(40，80，160 μmol/L)干预治疗，24 h 后进行检测。利用试剂盒检测川芎嗪对脂多糖诱导H9C2细胞乳酸脱氢酶以及活性氧释放的影响，荧光显微镜观察细胞凋亡情况，检测炎 症因子白细胞介素1β、肿瘤坏死因子α和白细胞介素6及Toll样受体4、MyD88的表达变化。 结果与结论： 与对照组比较，模型组细胞中乳酸脱氢酶、活性氧表达水平显著上升(P < 0.05)，荧光显微镜下观察发现大量细胞被PI染 色，且白细胞介素1β、肿瘤坏死因子α和白细胞介素6的表达水平显著升高(P < 0.05)；Toll样受体4、MyD88基因表达均显著上升(P < 0.05)； 与模型组比较，川芎嗪治疗组能够有效降低乳酸脱氢酶释放，降低活性氧水平，抑制PI染色H9C2细胞数目，降低白细胞介素1β、肿瘤 坏死因子α和白细胞介素6的表达水平，抑制Toll样受体4、MyD88 mRNA及蛋白的表达(P < 0.05)； 提示川芎嗪可能通过抑制Toll样受体4/ MyD88的表达降低细胞的炎症因子及氧化应激反应。 [ABSTRACT FROM AUTHOR]

: Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

العنوان البديل: Acupuncture and moxibustion combined with rehabilitation therapy improve neurological function and intestinal flora following cerebral ischemia in rats. (English)

المؤلفون: 崔振华, 林夏妃, 陈永敏, 林 烨, 李关羽, 宋振华

المصدر: Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu; 6/18/2023, Vol. 27 Issue 17, p2692-2698, 7p

مصطلحات موضوعية: HYDROCEPHALUS, CEREBRAL ischemia, LACTATE dehydrogenase, CAROTID artery, SUPEROXIDE dismutase, SCALP, CEREBRAL arteries

الملخص (بالإنجليزية): BACKGROUND: Both acupuncture and moxibustion and rehabilitation training can effectively alleviate the symptoms of patients with cerebral ischemia. At present, it is unclear whether the combined treatment of the two has a regulatory effect on neurological dysfunction and intestinal flora imbalance in patients with cerebral ischemia and its role mechanism. OBJECTIVE: To explore the effect of acupuncture and moxibustion combined with rehabilitation therapy on neurological function and intestinal flora in rats with cerebral ischemia. METHODS: Sixty Sprague-Dawley rats were randomly divided into sham operation group, model group, acupuncture group, rehabilitation group, and acupuncture+rehabilitation group (n=12 per group). Animal models of cerebral ischemia were prepared in all groups except for the sham operation group. In the sham operation group, the left common carotid artery was only separated but not ligated. The acupuncture group was treated with scalp cluster acupuncture intervention, the rehabilitation group was given task-oriented treadmill training, and the acupuncture+rehabilitation group was given scalp cluster acupuncture and task-oriented treadmill training intervention. Treatments in each group lasted for 14 days. The sham operation and model groups were not intervened. The neurological function was assessed by Longa score at 4 hours, 1, 7, and 14 days after modeling. Changes in brain water content were detected after 14 days of intervention. Western blot was applied to detect the expressions of neuron growth-related proteins (growth-associated protein 43, neurofilament 200, repulsive guidance molecule a) in the ischemic penumbra. Kit detection was used for detecting the levels of lactate dehydrogenase, superoxide dismutase, and malondialdehyde in brain tissue. ELISA was applied to detect the levels of tumor necrosis factor-α and interleukin-1β in brain tissue. Real-time fluorescent quantitative PCR was used to detect the changes of Escherichia coli, Bifidobacterium, Lactobacillus, and Enterococcus in rat feces. RESULTS AND CONCLUSION: At 4 hours, 1, 7, and 14 days after modeling, there was no neurological dysfunction in the sham operation group but obvious neurological dysfunction in the model group (P < 0.05). Compared with the model group, the neurological deficits of rats in the acupuncture and rehabilitation groups were significantly improved with the prolonged intervention time (P < 0.05), and the neurological function of rats in the acupuncture+rehabilitation group improved more significantly (P < 0.01). Compared with the model group, the expressions of growth-associated protein 43 and neurofilament 200 in the ischemic penumbra were significantly up-regulated in the acupuncture and rehabilitation groups (P < 0.05), the expression of repulsive guidance molecule a was significantly down-regulated (P < 0.05), the brain water content and levels of lactate dehydrogenase, malondialdehyde, tumor necrosis factor-α and interleukin-1β in brain tissue were reduced (P < 0.01), the superoxide dismutase level was raised (P < 0.01), the counts of Escherichia coli and Enterococcus in feces were significantly increased (P < 0.01), and the counts of Bifidobacterium and Lactobacillus were significantly decreased (P < 0.01). The above-mentioned indicators were improved more significantly in the acupuncture+rehabilitation group (P < 0.01). To conclude, acupuncture and moxibustion combined with rehabilitation therapy can improve neurological function, relieve oxidative stress and inflammatory responses, and regulate intestinal flora disorders in rats with cerebral ischemia by stimulating the regeneration of neurons in the ischemic penumbra. The combine therapy has a protective effect against ischemic stroke. [ABSTRACT FROM AUTHOR]

Abstract (Chinese): 背景：针灸与康复训练均能够有效缓解脑缺血患者症状，目前有关两者联合治疗是否对脑缺血患者神经功能障、肠道菌群失调具有调控作 用尚不明确。 目的：探究针灸联合康复疗法对脑缺血大鼠神经功能、肠道菌群的影响。 方法：将60只SD大鼠按随机数表法随机分为假手术组、模型组、针刺组、康复组和针康组(n=12)。除假手术组外，其余各组建立脑缺血大 鼠模型；假手术组仅分离左侧颈总动脉；针刺组用头穴丛刺干预，康复组进行任务导向性跑台训练，针康组同时给予头穴丛针刺和任务导 向性跑台训练干预，干预14 d。观察造模后4 h及1，7，14 d各组大鼠神经功能情况，检测干预14 d后大鼠脑含水量变化，Western blot检测 缺血半暗带神经元生长相关蛋白(生长相关蛋白43、神经丝蛋白200、排斥指导分子a)表达，试剂盒检测脑组织乳酸脱氢酶、超氧化物歧化 酶、丙二醛水平，酶联免疫吸附法检测脑组织肿瘤坏死因子α、白细胞介素1β质量浓度，实时荧光定量PCR检测大鼠粪便中大肠杆菌、双 歧杆菌、乳酸杆菌和肠球菌变化。 结果与结论：①造模后4 h及1，7，14 d，假手术组无神经功能障碍，模型组大鼠出现明显神经功能障碍(P < 0.05)；②与同时段模型组相 比，针刺组和康复组大鼠神经功能缺损随着干预时间延长有所改善(P < 0.05)，而针康组大鼠神经功能改善更显著(P < 0.01)；③与模型组比 较，针刺组、康复组大鼠缺血半暗带生长相关蛋白43、神经丝蛋白200表达上调(P < 0.05)，排斥指导分子a表达下调(P < 0.05)；大鼠脑组织 含水量和脑组织中乳酸脱氢酶、丙二醛、肿瘤坏死因子α、白细胞介素1β质量浓度降低(P < 0.05)，超氧化物歧化酶活性升高(P < 0.05)；粪 便中大肠杆菌、肠球菌数量明显增多(P < 0.05)，双歧杆菌、乳酸菌数量明显降低(P < 0.05)；且针康组上述指标改善更为显著(P < 0.01)；④ 提示针灸联合康复疗法可通过刺激缺血半暗带区神经元再生改善脑缺血大鼠神经功能，减轻氧化应激反应和炎症反应，调节肠道菌群紊 乱，对缺血性脑卒中具有保护作用。 [ABSTRACT FROM AUTHOR]

: Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

العنوان البديل: Protective mechanism of Naoxinqing Capsule in rat models of cerebral ischemia/reperfusion injury. (English)

المؤلفون: 闵冬雨, 李红岩, 关 乐, 常 江, 张海宁, 崔馨月, 王 鹏, 曹永刚

المصدر: Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu; 1/18/2020, Vol. 24 Issue 2, p215-222, 8p

مصطلحات موضوعية: NITRIC-oxide synthases, MONGOLIAN gerbil, CEREBRAL ischemia, REPERFUSION injury, LACTATE dehydrogenase, HIPPOCAMPUS (Brain), HINDLIMB, INTERLEUKIN-1

الملخص (بالإنجليزية): BACKGROUND: Naoxinqing capsule has been used for treating cerebral ischemia/reperfusion injury for a long time. However, there are relatively few in-depth studies on its mechanism. OBJECTIVE: To investigate the therapeutic effect of Naoxinqing Capsule on gerbil model of cerebral ischemia/reperfusion injury by molecular biological means. METHODS: The study was approved by the Laboratory Animal Ethical Committee of Liaoning University of Chinese Medicine, approval No. 21000092017072. Eighty male Mongolian gerbils were randomly divided into sham, model, Naoxinqing and Naoluotong groups, and the latter three groups underwent bilateral common carotid artery clip for 5 minutes, to establish the model of cerebral ischemia/reperfusion injury. The sham group received no common carotid artery clip. Next day, the sham group fed normally, the model group was given normal saline, Naoxinqing group was given the 100 mg/(kg•d) Naoxinqing via gavage, and Naoluotong group given 100 mg/(kg•d) Naoluotong via gavage, respectively, for 21 consecutive days. The water maze test was conducted at 1 week before experiment ended. The brain tissue was removed after experiment. The learning and memory function, hippocampal neurons, cerebrovascular and corresponding molecular changes were detected. RESULTS AND CONCLUSION: (1) Compared with the sham group, the learning ability in the model group was decreased significantly. Naoxinqing and Naoluotong groups could effectively improve the learning ability after surgery. (2) Compared with the model group, the numbers of neurons in the Naoxinqing and Naoluotong groups were increased significantly, arranged regularly with clear contour and complete structure. (3) Compared with the model group, in the Naoxinqing and Naoluotong groups, the activities of superoxide dismutase and lactate dehydrogenase, and glutathione content were significantly increased, and the content of malonaldehyde was significantly decreased (P < 0.01). (4) The expression levels of ASC, NLRP3 and Caspase-1 in the hippocampus in the Naoxinqing and Naoluotong groups were significantly lower than those in the model group (P < 0.05). (5) The levels of interleukin-18 and interleukin-1β in the Naoxinqing and Naoluotong groups were significantly lower than those in the model group (P < 0.01). (6) Compared with the model group, the cells positive for platelet endothelial cell adhesion molecule-1 in the Naoxinqing and Naoluotong groups were significantly increased, the cells contacted closely each other. (7) Compared with the model group, in the Naoxinqing and Naoluotong groups, the expression levels of platelet endothelial cell adhesion molecule-1 and phosphorylated endothelial nitric oxide synthase were significantly up-regulated, and the content of nitric oxide was significantly increased (P < 0.01). (8) These results indicate that Naoxinqing and Naoluotong can effectively protect the morphology of hippocampal CA1 region in gerbils. Cerebral ischemia/reperfusion injury is accompanied by cerebral vascular dysfunction. Naoxinqing Capsule can protect cerebral vascular function and inhibit cerebral ischemia/reperfusion injury. [ABSTRACT FROM AUTHOR]

Abstract (Chinese): 背景：脑心清胶囊用于脑缺血再灌注损伤的治疗由来已久，然而针对其作用机制的深入研究则相对较少。 目的：应用分子生物学手段考察脑心清胶囊对脑缺血再灌注损伤沙鼠模型的治疗作用。 方法：实验方案经辽宁中医药大学动物实验伦理委员会批准(批准号为21000092017072)。将 80 只雄性蒙古 沙鼠随机分为假手术组、模型组、脑心清组及脑络通组，后 3 组沙鼠应用无创微动脉夹同时夹闭双侧颈总动 脉5 min 后松开，建立脑缺血再灌注损伤模型；假手术组不夹闭双侧颈总动脉。术后次日开始假手术组正常 饲养，模型组灌服同体积的生理盐水，脑心清组按照100 mg/(kg•d)灌胃给药，脑络通组按照100 mg/(kg•d) 灌胃给药，连续给药 21 d。在实验结束前1 周进行水迷宫实验，实验结束后麻醉下处死沙鼠取脑组织。检测 沙鼠的学习记忆功能、海马神经元、脑血管及对应的分子变化情况。 结果与结论：①同假手术组相比，模型组沙鼠学习能力显著下降。而脑心清组及脑络通组则可有效提升术后 的学习能力下降趋势；②与模型组相比，脑心清组及脑络通组神经元显著增多，且排列较为整齐，细胞轮廓 清晰，结构完整；③与模型组相比，脑心清组及脑络通组沙鼠的超氧化物歧化酶和乳酸脱氢酶活性，谷胱甘 肽含量显著升高，丙二醛含量显著降低(P < 0.01)；④与模型组相比，脑心清组及脑络通组沙鼠海马组织ASC、 NLRP3 和 Caspase-1 蛋白表达下调(P < 0.05)；⑤与模型组相比，脑心清组及脑络通组沙鼠的白细胞介素18 和白细胞介素1β 含量明显降低(P < 0.01)；⑥与模型组相比，脑心清组及脑络通组沙鼠的血小板内皮细胞黏 附分子1 阳性细胞明显增多，细胞间连接紧密；⑦与模型组相比，脑心清组及脑络通组沙鼠海马组织血小板 内皮细胞黏附分子1 和磷酸化内皮型一氧化氮合酶表达显著上调，一氧化氮含量显著升高(P < 0.01)；⑧结果 说明，脑心清胶囊可有效保护沙鼠的海马CA1 区形态；脑缺血再灌注时伴有脑血管功能紊乱，脑心清胶囊可 以保护脑血管功能，进而抑制脑缺血再灌注损伤。 [ABSTRACT FROM AUTHOR]

: Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)