Objective:To determine the involvement and the modulatory effects of IL-33 during Plasmodium berghei ANKA(PbA)infection.Methods:PbA infection in male ICR mice was utilized as a model of malaria.Systemically circulatin...Objective:To determine the involvement and the modulatory effects of IL-33 during Plasmodium berghei ANKA(PbA)infection.Methods:PbA infection in male ICR mice was utilized as a model of malaria.Systemically circulating IL-33 levels were determined in blood plasma by enzyme-linked immunosorbent assay(ELISA).After 24 hours post-inoculation of PbA,recombinant IL-33 and ST2,and antibodies against IL-33 and IgG treatments were administered daily for 3 days.Tissue expression and localization of IL-33 were assessed in organs generally affected by malaria via immunohistochemistry.Moreover,histopathological examination was performed to assess the effects of the treatments.Results:The levels of systemic IL-33 were elevated at the critical phase of PbA infection.Likewise,immunohistochemical analysis revealed a significant upregulation of IL-33 expression at the critical phase in the brain,lungs,and spleen of PbA-infected mice as compared to healthy controls.Treatment with IL-33 protected against experimental cerebral malaria development and reduced pathological features in the brain and lungs of the PbA-infected mice.Conclusions:A potential critical role and involvement of IL-33 in PbA infection may hint at the resolution of immunopathological sequelae associated with malaria.展开更多
Morphine is a schedule II-controlled substance that used to allow the diminution of intra-operative, post-operative orchronic pain. However, its usage is limited due to addiction and overdose liabilities. Morphine was...Morphine is a schedule II-controlled substance that used to allow the diminution of intra-operative, post-operative orchronic pain. However, its usage is limited due to addiction and overdose liabilities. Morphine was observed to cause tolerance,dependence and withdrawal in human. Justification: to date lack of scientific evidence of morphine addiction was carried out byusing specific single human neuroblastoma cell-line (SK-N-SH). Therefore, this study was performed to establish the morphineaddiction model in this cell line. The cells were exposed to morphine for 24 hrs before treatment with methadone, as ananti-withdrawal drug for subsequence 24 hours. The cytosolic fraction of the cell was used in different objectives including receptoraffinity, withdrawal properties, endocytic machinery, desensitisation or internalisation and cellular adaptation. The result shows thatmorphine and methadone bind to the μ-opioid receptor. The morphine-treated cells were observed to increase the expression ofaddiction markers, have a low rate of the endocytic machinery, cause desensitisation of receptor and reduce cellular adaptation.Those changes by morphine were normalised by the treatment of methadone. As a whole, it is postulated that neuroblastoma cell line,SK-N-SH, can be used as an in-vitro model to demonstrate morphine addiction before animal and human testing.展开更多
基金supported by the Fundamental Research Grant Scheme(FRGS)from the Malaysia Ministry of Higher Education(FRGS/1/2016/SKK10/UPM/02/1).
文摘Objective:To determine the involvement and the modulatory effects of IL-33 during Plasmodium berghei ANKA(PbA)infection.Methods:PbA infection in male ICR mice was utilized as a model of malaria.Systemically circulating IL-33 levels were determined in blood plasma by enzyme-linked immunosorbent assay(ELISA).After 24 hours post-inoculation of PbA,recombinant IL-33 and ST2,and antibodies against IL-33 and IgG treatments were administered daily for 3 days.Tissue expression and localization of IL-33 were assessed in organs generally affected by malaria via immunohistochemistry.Moreover,histopathological examination was performed to assess the effects of the treatments.Results:The levels of systemic IL-33 were elevated at the critical phase of PbA infection.Likewise,immunohistochemical analysis revealed a significant upregulation of IL-33 expression at the critical phase in the brain,lungs,and spleen of PbA-infected mice as compared to healthy controls.Treatment with IL-33 protected against experimental cerebral malaria development and reduced pathological features in the brain and lungs of the PbA-infected mice.Conclusions:A potential critical role and involvement of IL-33 in PbA infection may hint at the resolution of immunopathological sequelae associated with malaria.
文摘Morphine is a schedule II-controlled substance that used to allow the diminution of intra-operative, post-operative orchronic pain. However, its usage is limited due to addiction and overdose liabilities. Morphine was observed to cause tolerance,dependence and withdrawal in human. Justification: to date lack of scientific evidence of morphine addiction was carried out byusing specific single human neuroblastoma cell-line (SK-N-SH). Therefore, this study was performed to establish the morphineaddiction model in this cell line. The cells were exposed to morphine for 24 hrs before treatment with methadone, as ananti-withdrawal drug for subsequence 24 hours. The cytosolic fraction of the cell was used in different objectives including receptoraffinity, withdrawal properties, endocytic machinery, desensitisation or internalisation and cellular adaptation. The result shows thatmorphine and methadone bind to the μ-opioid receptor. The morphine-treated cells were observed to increase the expression ofaddiction markers, have a low rate of the endocytic machinery, cause desensitisation of receptor and reduce cellular adaptation.Those changes by morphine were normalised by the treatment of methadone. As a whole, it is postulated that neuroblastoma cell line,SK-N-SH, can be used as an in-vitro model to demonstrate morphine addiction before animal and human testing.
