Objective:To observe the serum levels of Fibrinogen(Fg),Interleukin-33(IL-33)in patients with cerebral infarction and periodontitis,and to explore the relationship of cerebral infarction and periodontitis.Methods:104 ...Objective:To observe the serum levels of Fibrinogen(Fg),Interleukin-33(IL-33)in patients with cerebral infarction and periodontitis,and to explore the relationship of cerebral infarction and periodontitis.Methods:104 subjects were included in this study.Among them,23 were patients with CI and CP(group CI+CP),28 with CI(group CI),28 with CP(group CP)and 25 were healthy volunteers(group H).The periodontal indexes and the serum levels of Fg and IL-33 were measured.Results:In groups of CI+CP,CP and CI the Fg and IL-33 were significantly higher than those in the group H(P<0.01).In groups of CI+CP the Fg and Il-33 was higher than group CI and CP(P<0.05).Conclusion:In patients with cerebral infarction with periodontitis,the levels of fibrinogen and interleukin-33 were both increased,and their concentrations were in direct proportion to the periodontal indexes。展开更多
ObjectiveTo understand the pathogenetic role and clinical significance of interleukin 6(IL -6),tumor necrosis factor(TNF)and soluble interleukin -2receptor(sIL -2R)in patients with cerebral infarctio n(CI ).MethodsThe...ObjectiveTo understand the pathogenetic role and clinical significance of interleukin 6(IL -6),tumor necrosis factor(TNF)and soluble interleukin -2receptor(sIL -2R)in patients with cerebral infarctio n(CI ).MethodsThe IL -6,TNF and sIL -2R levels were measured in 46CI patient s with ELISA.ResultsThe serum IL -6,TNF and sIL -2R levels of CI group were much higher than those of controls group .The variation of IL -6,TNF and sIL -2R levels was c losely related to the size of cerebra l infarction.The serum IL -6,TNF and sIL -2R levels of recovery p eriod were much lower than those of acute period in patients with CI .Conclusions The IL -6,TNF and sIL -2R take part in the pathologi c process after CI .The measurement o f IL -6,TNF and sIL -2R is useful in determining the size of cerebral infarction.展开更多
Interleukin-4(IL-4) has a protective effect against cerebral ischemia/reperfusion injury. Animal experiments have shown that IL-4 improves the short-and long-term prognosis of neurological function. The Akt(also calle...Interleukin-4(IL-4) has a protective effect against cerebral ischemia/reperfusion injury. Animal experiments have shown that IL-4 improves the short-and long-term prognosis of neurological function. The Akt(also called protein kinase B, PKB)/glycogen synthase kinase-3β(Akt/GSK-3β) signaling pathway is involved in oxidative stress, the inflammatory response, apoptosis, and autophagy. However, it is not yet clear whether the Akt/GSK-3β pathway participates in the neuroprotective effect of IL-4 against cerebral ischemia/reperfusion injury. In the present study, we established a cerebral ischemia/reperfusion mouse model by middle cerebral artery occlusion for 60 minutes followed by a 24-hour reperfusion. An IL-4/anti-IL-4 complex(10 μg) was intraperitoneally administered 30 minutes before surgery. We found that administration of IL-4 significantly alleviated the neurological deficits, oxidative stress, cell apoptosis, and autophagy and reduced infarct volume of the mice with cerebral ischemia/reperfusion injury 24 hours after reperfusion. Simultaneously, IL-4 activated Akt/GSK-3β signaling pathway. However, an Akt inhibitor LY294002, which was injected at 15 nmol/kg via the tail vein, attenuated the protective effects of IL-4. These findings indicate that IL-4 has a protective effect on cerebral ischemia/reperfusion injury by mitigating oxidative stress, reducing apoptosis, and inhibiting excessive autophagy, and that this mechanism may be related to activation of the Akt/GSK-3β pathway. This animal study was approved by the Animal Ethics Committee of Renmin Hospital of Wuhan University, China(approval No. WDRY2017-K037) on March 9, 2017.展开更多
BACKGROUND： Previous studies have confirmed the neuroprotective effect of mild hypothermia on ischemic brain injury. OBJECTIVE： To investigate the effects of mild hypothermia on intercellular adhesion molecule-1 exp...BACKGROUND： Previous studies have confirmed the neuroprotective effect of mild hypothermia on ischemic brain injury. OBJECTIVE： To investigate the effects of mild hypothermia on intercellular adhesion molecule-1 expression and serum interleukin-6 levels in ischemic brain tissues of focal brain ischemia rats, and to explore the neuroprotective effects of mild hypothermia on ischemic brain injury. DESIGN, TIME AND SETTING： A randomized, controlled, neurobiological experiment was performed at the Central Laboratory, First Affiliated Hospital, Xinxiang Medical College, China from February to July 2006. MATERIALS： Thirty healthy, adult, Sprague Dawley rats were used to establish middle cerebral artery occlusion models using the suture method, The immunohistochemistry （streptavidin-biotin-peroxidase complex method） kit was purchased from Boster, China. Interleukin-6 radioimmunoassay was supplied by Institute of Radioimmunity, Technology Development Center, General Hospital of Chinese PLA. METHODS： The rats were equally and randomly assigned into mild hypothermia and control groups, and middle cerebral artery occlusion models were established. The rectal temperature was maintained at （37 ±0.5）℃ in the control group. In the mild hypothermia group, the rectal temperature was maintained at （33±1）℃. MAIN OUTCOME MEASURES： At 12 hours after model establishment, the ischemic brain hemispheres were coronally sliced at the level of the optic chiasm. The number of intercellular adhesion molecule-1-positive vessels per high-power field was observed with an optical microscope. Serum interleukin-6 levels were measured by radioimmunoassay. RESULTS： Compared with the control group, intercellular adhesion molecule-1 and serum interleukin-6 expressions were significantly decreased in ischemic brain tissues of the mild hypothermia group （P 〈 0.01）. CONCLUSION： Mild hypothermia exhibits a neuroprotective effect by reducing serum interleukin-6 and intercellular adhesion molecule-1 expression following cerebral ischemia.展开更多
Objectives To examine effect of atorvastatin on the expression of COX-2 in peripheral blood monocytes from patients with early stage of acute myocardial infarction (AMI) in vitro, and the IL-6 concentration in superna...Objectives To examine effect of atorvastatin on the expression of COX-2 in peripheral blood monocytes from patients with early stage of acute myocardial infarction (AMI) in vitro, and the IL-6 concentration in supernatant was also examined. Methods Patients with AMI (n=40) and with stable coronary heart disease (CHD) (n=18) were registered. Peripheral blood monocytes from all participants were isolated and cultured for 24 hrs, but those from patients with AMI were randomly exposed to various concentration of atorvastatin (0, 0.1, 1, 10 μmol/L) during the cultivation. COX-2 mRNA expression in monocytes was analyzed by reverse transcription polymerase chain reaction (RT-PCR). Concentration of IL-6 in supernatant was measured by enzyme-linked immunosorbent assay (ELISA). Results COX-2 expression and IL-6 secretion by peripheral blood monocytes from patients with AMI (0.92±0.13, 205±46 pg/ml) were higher than that from controls (0.19±0.08, 41±8 pg/ml) (both P<0.05), and COX-2 expression was dramatically reduced up to 52% by atorvastatin (P<0.05), in a concentration-dependent manner respectively. The expression of COX-2 from patients with AMI was obviously correlated with the secretion of IL-6 (r=0.636, P<0.05). COX-2 expression in the monocytes after intervention of atorvastatin was also positively correlated with IL-6 secretion by these cells (r=0.783, P<0.05). Conclusions COX-2 involves inflammatory respond in early-stage of AMI. Atorvastatin may decrease COX-2 expression in peripheral blood monocytes from patients with AMI and cyclooxygenase-dependent pathway might be correlated with the anti-inflammation mechanism of statin.展开更多
Objective： To investigate the effects of acupuncture therapy on acute cerebral infarction. Methods： Eighty patients with acute cerebral infarction were randomly divided into a treatment group of 40 cases and a contr...Objective： To investigate the effects of acupuncture therapy on acute cerebral infarction. Methods： Eighty patients with acute cerebral infarction were randomly divided into a treatment group of 40 cases and a control group of 40 cases. Xuanzhong（GB 39）-throughSanyinjiao（SP 6） acupuncture was performed as a main treatment. The curative effects were compared between the two groups and the sizes of cerebral infarct, between pretreatment and posttreatment after one course of treatment. Results. The total recovery rate was 88.5% in the treatment group and 57.5% in the control group after one course of treatment. There was a significant difference between the two（P〈 0.05）. The rate of change in the infarct for the better was significantly higher in the treatment group than in the control group. There was also a significant difference（P〈 0.05）, Conclusion： This treatment is an effective method for lowering the rate of apoplectic disability and raising the cure rate,展开更多
基金Natural science fund project of Hainan Province(No.819MS125)。
文摘Objective:To observe the serum levels of Fibrinogen(Fg),Interleukin-33(IL-33)in patients with cerebral infarction and periodontitis,and to explore the relationship of cerebral infarction and periodontitis.Methods:104 subjects were included in this study.Among them,23 were patients with CI and CP(group CI+CP),28 with CI(group CI),28 with CP(group CP)and 25 were healthy volunteers(group H).The periodontal indexes and the serum levels of Fg and IL-33 were measured.Results:In groups of CI+CP,CP and CI the Fg and IL-33 were significantly higher than those in the group H(P<0.01).In groups of CI+CP the Fg and Il-33 was higher than group CI and CP(P<0.05).Conclusion:In patients with cerebral infarction with periodontitis,the levels of fibrinogen and interleukin-33 were both increased,and their concentrations were in direct proportion to the periodontal indexes。
文摘ObjectiveTo understand the pathogenetic role and clinical significance of interleukin 6(IL -6),tumor necrosis factor(TNF)and soluble interleukin -2receptor(sIL -2R)in patients with cerebral infarctio n(CI ).MethodsThe IL -6,TNF and sIL -2R levels were measured in 46CI patient s with ELISA.ResultsThe serum IL -6,TNF and sIL -2R levels of CI group were much higher than those of controls group .The variation of IL -6,TNF and sIL -2R levels was c losely related to the size of cerebra l infarction.The serum IL -6,TNF and sIL -2R levels of recovery p eriod were much lower than those of acute period in patients with CI .Conclusions The IL -6,TNF and sIL -2R take part in the pathologi c process after CI .The measurement o f IL -6,TNF and sIL -2R is useful in determining the size of cerebral infarction.
基金supported by the National Natural Science Foundation of China,Nos.81901994(to BZ)and 81571147(to XXX)the Natural Science Foundation of Hubei Province,China,No.2019CFC847(to WWG)the Fundamental Research Funds for the Central Universities,China,No.2042018kf0149(to ML)
文摘Interleukin-4(IL-4) has a protective effect against cerebral ischemia/reperfusion injury. Animal experiments have shown that IL-4 improves the short-and long-term prognosis of neurological function. The Akt(also called protein kinase B, PKB)/glycogen synthase kinase-3β(Akt/GSK-3β) signaling pathway is involved in oxidative stress, the inflammatory response, apoptosis, and autophagy. However, it is not yet clear whether the Akt/GSK-3β pathway participates in the neuroprotective effect of IL-4 against cerebral ischemia/reperfusion injury. In the present study, we established a cerebral ischemia/reperfusion mouse model by middle cerebral artery occlusion for 60 minutes followed by a 24-hour reperfusion. An IL-4/anti-IL-4 complex(10 μg) was intraperitoneally administered 30 minutes before surgery. We found that administration of IL-4 significantly alleviated the neurological deficits, oxidative stress, cell apoptosis, and autophagy and reduced infarct volume of the mice with cerebral ischemia/reperfusion injury 24 hours after reperfusion. Simultaneously, IL-4 activated Akt/GSK-3β signaling pathway. However, an Akt inhibitor LY294002, which was injected at 15 nmol/kg via the tail vein, attenuated the protective effects of IL-4. These findings indicate that IL-4 has a protective effect on cerebral ischemia/reperfusion injury by mitigating oxidative stress, reducing apoptosis, and inhibiting excessive autophagy, and that this mechanism may be related to activation of the Akt/GSK-3β pathway. This animal study was approved by the Animal Ethics Committee of Renmin Hospital of Wuhan University, China(approval No. WDRY2017-K037) on March 9, 2017.
文摘BACKGROUND： Previous studies have confirmed the neuroprotective effect of mild hypothermia on ischemic brain injury. OBJECTIVE： To investigate the effects of mild hypothermia on intercellular adhesion molecule-1 expression and serum interleukin-6 levels in ischemic brain tissues of focal brain ischemia rats, and to explore the neuroprotective effects of mild hypothermia on ischemic brain injury. DESIGN, TIME AND SETTING： A randomized, controlled, neurobiological experiment was performed at the Central Laboratory, First Affiliated Hospital, Xinxiang Medical College, China from February to July 2006. MATERIALS： Thirty healthy, adult, Sprague Dawley rats were used to establish middle cerebral artery occlusion models using the suture method, The immunohistochemistry （streptavidin-biotin-peroxidase complex method） kit was purchased from Boster, China. Interleukin-6 radioimmunoassay was supplied by Institute of Radioimmunity, Technology Development Center, General Hospital of Chinese PLA. METHODS： The rats were equally and randomly assigned into mild hypothermia and control groups, and middle cerebral artery occlusion models were established. The rectal temperature was maintained at （37 ±0.5）℃ in the control group. In the mild hypothermia group, the rectal temperature was maintained at （33±1）℃. MAIN OUTCOME MEASURES： At 12 hours after model establishment, the ischemic brain hemispheres were coronally sliced at the level of the optic chiasm. The number of intercellular adhesion molecule-1-positive vessels per high-power field was observed with an optical microscope. Serum interleukin-6 levels were measured by radioimmunoassay. RESULTS： Compared with the control group, intercellular adhesion molecule-1 and serum interleukin-6 expressions were significantly decreased in ischemic brain tissues of the mild hypothermia group （P 〈 0.01）. CONCLUSION： Mild hypothermia exhibits a neuroprotective effect by reducing serum interleukin-6 and intercellular adhesion molecule-1 expression following cerebral ischemia.
文摘Objectives To examine effect of atorvastatin on the expression of COX-2 in peripheral blood monocytes from patients with early stage of acute myocardial infarction (AMI) in vitro, and the IL-6 concentration in supernatant was also examined. Methods Patients with AMI (n=40) and with stable coronary heart disease (CHD) (n=18) were registered. Peripheral blood monocytes from all participants were isolated and cultured for 24 hrs, but those from patients with AMI were randomly exposed to various concentration of atorvastatin (0, 0.1, 1, 10 μmol/L) during the cultivation. COX-2 mRNA expression in monocytes was analyzed by reverse transcription polymerase chain reaction (RT-PCR). Concentration of IL-6 in supernatant was measured by enzyme-linked immunosorbent assay (ELISA). Results COX-2 expression and IL-6 secretion by peripheral blood monocytes from patients with AMI (0.92±0.13, 205±46 pg/ml) were higher than that from controls (0.19±0.08, 41±8 pg/ml) (both P<0.05), and COX-2 expression was dramatically reduced up to 52% by atorvastatin (P<0.05), in a concentration-dependent manner respectively. The expression of COX-2 from patients with AMI was obviously correlated with the secretion of IL-6 (r=0.636, P<0.05). COX-2 expression in the monocytes after intervention of atorvastatin was also positively correlated with IL-6 secretion by these cells (r=0.783, P<0.05). Conclusions COX-2 involves inflammatory respond in early-stage of AMI. Atorvastatin may decrease COX-2 expression in peripheral blood monocytes from patients with AMI and cyclooxygenase-dependent pathway might be correlated with the anti-inflammation mechanism of statin.
文摘Objective： To investigate the effects of acupuncture therapy on acute cerebral infarction. Methods： Eighty patients with acute cerebral infarction were randomly divided into a treatment group of 40 cases and a control group of 40 cases. Xuanzhong（GB 39）-throughSanyinjiao（SP 6） acupuncture was performed as a main treatment. The curative effects were compared between the two groups and the sizes of cerebral infarct, between pretreatment and posttreatment after one course of treatment. Results. The total recovery rate was 88.5% in the treatment group and 57.5% in the control group after one course of treatment. There was a significant difference between the two（P〈 0.05）. The rate of change in the infarct for the better was significantly higher in the treatment group than in the control group. There was also a significant difference（P〈 0.05）, Conclusion： This treatment is an effective method for lowering the rate of apoplectic disability and raising the cure rate,
