Several experimental evidence suggests a link between brain Herpes simplex virus type-1 infection and the occurrence of Alzheimer’s disease.However,the molecular mechanisms underlying this association are not complet...Several experimental evidence suggests a link between brain Herpes simplex virus type-1 infection and the occurrence of Alzheimer’s disease.However,the molecular mechanisms underlying this association are not completely understood.Among the molecular mediators of synaptic and cognitive dysfunction occurring after Herpes simplex virus type-1 infection and reactivation in the brain neuroinflammatory cytokines seem to occupy a central role.Here,we specifically reviewed literature reports dealing with the impact of neuroinflammation on synaptic dysfunction observed after recurrent Herpes simplex virus type-1 reactivation in the brain,highlighting the role of interleukins and,in particular,interleukin 1βas a possible target against Herpes simplex virus type-1-induced neuronal dysfunctions.展开更多
BACKGROUND： Interleukin 1β-converting enzyme （ICE） gene expression can induce neuronal apoptosis. However, the dynamic changes in ICE gene expression and its effects on neuronal apoptosis under cerebral ischemia/r...BACKGROUND： Interleukin 1β-converting enzyme （ICE） gene expression can induce neuronal apoptosis. However, the dynamic changes in ICE gene expression and its effects on neuronal apoptosis under cerebral ischemia/reperfusion conditions remain unclear. OBJECTIVE： To observe neuronal apoptosis and changes in ICE gene expression in the frontal cortex and hippocampus following ischemia/reperfusion injury. DESIGN, TIME AND SETTING： A randomized, controlled animal study was conducted at the Laboratory of Experimental Animal Center, the Second Hospital of Jilin University and Central Laboratory, the Second Hospital of Jilin University, China, from November 2008 to September 2009. MATERIALS： The ICE gene primer sequence （TaKaPa Co., Dalian, China）, FACScan Flow cytometer （Becton Dickinson, Franklin Lakes, N J, USA）, and Perkin Elmer GeneAmp PCR system 2400 （Perkin Elmer, Waltham, MA, USA） were used in this study. METHODS： A total of 45 healthy, adult, male, Kunming mice were randomly assigned to normal control （n = 5）, sham surgery （n = 5）, and model （n = 35） groups. The mice in the model group were equally and randomly subdivided into seven subgroups according to various reperfusion time points （1 hour, 1,3, 7, 14, 28, and 42 days）. Animal models of ischemia/reperfusion injury were established by bilateral carotid artery ligation in the model group. The mice in the sham surgery group only received saline perfusion and surgery for carotid artery exposure. MAIN OUTCOME MEASURES： Neuronal apoptosis in the frontal cortex and hippocampus of mice was measured using flow cytometry. The time course of ICE mRNA levels in the frontal cortex and hippocampus were quantified using reverse transcription-polymerase chain reaction. RESULTS： Neuronal apoptosis in the frontal cortex and hippocampus peaked at 3 days following ischemia/reperfusion injury （P 〈 0.05）. ICE mRNA expression increased in the frontal cortex at 1 day following ischemia/reperfusion injury （P 〈 0.05）, decreased at 3 days, and then peaked at 14 days （P 〈 0.05）. ICE mRNA expression increased in the hippocampus at 3 days following ischemia/reperfusion injury （P 〈 0.05）, peaked at 7 days （P 〈 0.05）, and then decreased gradually to normal levels at 28 days. CONCLUSION： Neuronal apoptosis peaked at 3 days following ischemia/reperfusion injury, and both apoptosis and ICE mRNA levels remained high for 2 weeks after injury. Early apoptosis may result from increased ICE mRNA expression.展开更多
Purpose. To study the interleukin 1 (IL-1)levels in aqueous humor after transscleral fixation of in- traocular lenses (IOLs) implantation in rabbits and discuss the effect of IL-1 on postoperative anterior ocular infl...Purpose. To study the interleukin 1 (IL-1)levels in aqueous humor after transscleral fixation of in- traocular lenses (IOLs) implantation in rabbits and discuss the effect of IL-1 on postoperative anterior ocular inflammation. Methods. Twenty-seven pigmented rabbits were divided into three groups: GI, transscleral fixation of posterior chamber (PC) IOLs implantation; G2, Lens of rabbits were removed without IOLs implanta- tion; G3, the control group, without surgical intervention. On the 1st, 3rd, 7th and 14th postoperative days, aqueous humor samples were obtained. Methyl thiazolyl tetrazolium (MTT) colormetry was used to detected for the presence of IL-1. The data were analyzed by using analysis of variance of SAS soft ware. Results’ It was found that IL-1 level in aqueous humor was increased after transscleral fixation of I- OLs implantation, IL-1 level reached its maximum on the 14th postoperative days in the IOL implanted group. IL-1 levels on 1st, 3rd, 7th and 14th days postoperatively was significantly higher (P<0. 05) in I- OLs implanted group than that of only extracapsular lenses extraction but no IOLs implantation group and that of the none surgical intervention group. COnclusions.IL-1 levels increased had a close relationship with a specific response to IOL implanta- tion. The increase of IL-1 may be suggested as the principal mediators of immunological and inflammatory responses, so that may play critical role in anterior ocular inflammative response after IOL implantation.展开更多
The in vivo effects of Phytolacca acinosa poly-saccharides I (PEP-I) on immunologic cytotoxicity of mouse peritoneal macrophages and its production of tumor necrosis factor (TNF) and interleukin 1 (IL-1) were studied....The in vivo effects of Phytolacca acinosa poly-saccharides I (PEP-I) on immunologic cytotoxicity of mouse peritoneal macrophages and its production of tumor necrosis factor (TNF) and interleukin 1 (IL-1) were studied. PEP-I 80 or 160 mg kg was given ip twice every 4 day. Both doses were found to have significant enhancing activity on macrophages cytotoxicity against S180 sarcoma cells and malignant transformed fibroblast L929 cells. Peritoneal activated macrophages were incubated with LPS for 2 and 24 hrs to induce TNF and IL-1, respectively. The TNF and IL-1 activities were tested from cytotoxicity against L929 cells in an absorbence assay of enzymatic reaction and proliferation of thymocytes co-stimulated assay separately. The optimal time for TNF production was found on day 8. Significant increases in TNF and IL-1 were observed. In comparison of the effect of PEP-I on TNF with that of known priming agent BCG, there was no difference between them, but PEP-I had a high effect on IL-1. These results suggest that cytotoxicity of macrophages primed by PEP-I is closely related to its TNF and IL-1 production.展开更多
基金supported by UniversitàCattolica(D1 intramural funds to RP)Italian Ministry of University and Research(PRIN 2022ZYLB7B,P2022YW7BP funds to CG).
文摘Several experimental evidence suggests a link between brain Herpes simplex virus type-1 infection and the occurrence of Alzheimer’s disease.However,the molecular mechanisms underlying this association are not completely understood.Among the molecular mediators of synaptic and cognitive dysfunction occurring after Herpes simplex virus type-1 infection and reactivation in the brain neuroinflammatory cytokines seem to occupy a central role.Here,we specifically reviewed literature reports dealing with the impact of neuroinflammation on synaptic dysfunction observed after recurrent Herpes simplex virus type-1 reactivation in the brain,highlighting the role of interleukins and,in particular,interleukin 1βas a possible target against Herpes simplex virus type-1-induced neuronal dysfunctions.
文摘BACKGROUND： Interleukin 1β-converting enzyme （ICE） gene expression can induce neuronal apoptosis. However, the dynamic changes in ICE gene expression and its effects on neuronal apoptosis under cerebral ischemia/reperfusion conditions remain unclear. OBJECTIVE： To observe neuronal apoptosis and changes in ICE gene expression in the frontal cortex and hippocampus following ischemia/reperfusion injury. DESIGN, TIME AND SETTING： A randomized, controlled animal study was conducted at the Laboratory of Experimental Animal Center, the Second Hospital of Jilin University and Central Laboratory, the Second Hospital of Jilin University, China, from November 2008 to September 2009. MATERIALS： The ICE gene primer sequence （TaKaPa Co., Dalian, China）, FACScan Flow cytometer （Becton Dickinson, Franklin Lakes, N J, USA）, and Perkin Elmer GeneAmp PCR system 2400 （Perkin Elmer, Waltham, MA, USA） were used in this study. METHODS： A total of 45 healthy, adult, male, Kunming mice were randomly assigned to normal control （n = 5）, sham surgery （n = 5）, and model （n = 35） groups. The mice in the model group were equally and randomly subdivided into seven subgroups according to various reperfusion time points （1 hour, 1,3, 7, 14, 28, and 42 days）. Animal models of ischemia/reperfusion injury were established by bilateral carotid artery ligation in the model group. The mice in the sham surgery group only received saline perfusion and surgery for carotid artery exposure. MAIN OUTCOME MEASURES： Neuronal apoptosis in the frontal cortex and hippocampus of mice was measured using flow cytometry. The time course of ICE mRNA levels in the frontal cortex and hippocampus were quantified using reverse transcription-polymerase chain reaction. RESULTS： Neuronal apoptosis in the frontal cortex and hippocampus peaked at 3 days following ischemia/reperfusion injury （P 〈 0.05）. ICE mRNA expression increased in the frontal cortex at 1 day following ischemia/reperfusion injury （P 〈 0.05）, decreased at 3 days, and then peaked at 14 days （P 〈 0.05）. ICE mRNA expression increased in the hippocampus at 3 days following ischemia/reperfusion injury （P 〈 0.05）, peaked at 7 days （P 〈 0.05）, and then decreased gradually to normal levels at 28 days. CONCLUSION： Neuronal apoptosis peaked at 3 days following ischemia/reperfusion injury, and both apoptosis and ICE mRNA levels remained high for 2 weeks after injury. Early apoptosis may result from increased ICE mRNA expression.
文摘Purpose. To study the interleukin 1 (IL-1)levels in aqueous humor after transscleral fixation of in- traocular lenses (IOLs) implantation in rabbits and discuss the effect of IL-1 on postoperative anterior ocular inflammation. Methods. Twenty-seven pigmented rabbits were divided into three groups: GI, transscleral fixation of posterior chamber (PC) IOLs implantation; G2, Lens of rabbits were removed without IOLs implanta- tion; G3, the control group, without surgical intervention. On the 1st, 3rd, 7th and 14th postoperative days, aqueous humor samples were obtained. Methyl thiazolyl tetrazolium (MTT) colormetry was used to detected for the presence of IL-1. The data were analyzed by using analysis of variance of SAS soft ware. Results’ It was found that IL-1 level in aqueous humor was increased after transscleral fixation of I- OLs implantation, IL-1 level reached its maximum on the 14th postoperative days in the IOL implanted group. IL-1 levels on 1st, 3rd, 7th and 14th days postoperatively was significantly higher (P<0. 05) in I- OLs implanted group than that of only extracapsular lenses extraction but no IOLs implantation group and that of the none surgical intervention group. COnclusions.IL-1 levels increased had a close relationship with a specific response to IOL implanta- tion. The increase of IL-1 may be suggested as the principal mediators of immunological and inflammatory responses, so that may play critical role in anterior ocular inflammative response after IOL implantation.
文摘The in vivo effects of Phytolacca acinosa poly-saccharides I (PEP-I) on immunologic cytotoxicity of mouse peritoneal macrophages and its production of tumor necrosis factor (TNF) and interleukin 1 (IL-1) were studied. PEP-I 80 or 160 mg kg was given ip twice every 4 day. Both doses were found to have significant enhancing activity on macrophages cytotoxicity against S180 sarcoma cells and malignant transformed fibroblast L929 cells. Peritoneal activated macrophages were incubated with LPS for 2 and 24 hrs to induce TNF and IL-1, respectively. The TNF and IL-1 activities were tested from cytotoxicity against L929 cells in an absorbence assay of enzymatic reaction and proliferation of thymocytes co-stimulated assay separately. The optimal time for TNF production was found on day 8. Significant increases in TNF and IL-1 were observed. In comparison of the effect of PEP-I on TNF with that of known priming agent BCG, there was no difference between them, but PEP-I had a high effect on IL-1. These results suggest that cytotoxicity of macrophages primed by PEP-I is closely related to its TNF and IL-1 production.
