Background: Tuberculosis (TB) is one of the world’s deadliest infectious diseases. Tumor necrosis factor-Alpha (TNF-α) and Interleukin 8 (IL-8) are involved in the pathogenesis of pulmonary TB (PTB). However, the co...Background: Tuberculosis (TB) is one of the world’s deadliest infectious diseases. Tumor necrosis factor-Alpha (TNF-α) and Interleukin 8 (IL-8) are involved in the pathogenesis of pulmonary TB (PTB). However, the contribution of polymorphisms of these cytokines to PTB susceptibility needed more investigation across geographic regions and ethnic groups. Purpose: The aim of this study was to investigate the association of the TNF-α-308 G/A and IL-8-251T/A polymorphisms with PTB risk in the Congolese population. Methods: This case-control study included 150 PTB patients and 160 control subjects. Blood samples were collected from all participants and were used for the TNF-α-308 G/A and IL-8-251T/A genotyping by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique. Odds ratios (OR) were calculated to estimate the potential polymorphism associations. A P level of Results: A significant difference was found between PTB patients and controls regarding the TNF-α-308AA genotype (P = 0.035) distribution. Moreover, this genotype was associated with risk to TB (OR = 7.19, 95% CI = 0.85 - 60.65, P = 0.035). The A allele was significantly more frequent in PTB patients than in controls, and was associated with risk to PTB (OR = 1.68, 95% CI = 1.05 - 2.68, P = 0.014). Regarding the IL-8-251T/A gene, TA and AA genotypes were significantly more frequent in PTB patients compared to controls, and were associated with increased risk to PTB (OR = 2.64, 95% CI = 0.97 - 7.18, P = 0.031 and OR = 3.0, 95% CI = 1.13 - 7.98, P = 0.014, respectively). However, the IL-8-251 A allele was not associated to PTB susceptibility (OR = 0.27, 95% CI = 0.15 - 0.44). Conclusion: TNF-α-308G/A and IL-8-251T/A polymorphisms may be associated to PTB susceptibility in the Congolese population, and the AA genotype of both cytokines could be a risk factor.展开更多
Objective:To summarize the precise association between pulmonary tuberculosis(PTB) and P2x7 A1513 C gene polymorphism.Methods:PubMed and Google Scholar web-databases were searched for the studies reporting the associa...Objective:To summarize the precise association between pulmonary tuberculosis(PTB) and P2x7 A1513 C gene polymorphism.Methods:PubMed and Google Scholar web-databases were searched for the studies reporting the association of P2x7 A1513 C polymorphism and PTB risk.A meta-analysis was performed for the selected case-control studies and pooled odds ratios(ORs) and 95%confidence intervals(95%CIs) were calculated for all the genetic models.Results:Eleven studies comprising 2 678 controls and 2 113 PTB cases were included in this meta-analysis.We observed overall no significant risk in all the five genetic models.When stratified population by the ethnicity,Caucasian population failed to show any risk of PTB in all the genetics models.In Asian ethnicity,variant allele(C vs.A:P=0.001;QR=1.375,95%CI=1.159-1.632) and heterozygous genotype(AC vs.AA:P=0.001;OR=1.570,95%CI=1.269-1.944) demonstrated significant increased risk of PTB.Likewise,recessive genetic model(CC+AC vs.AA:P=0.001;OR=1.540,95%CI= 1.255-1.890) also demonstrated increased risk of PTB in Asians.Conclusions:Our meta-analysis did not suggest the association of P2x7 A1513 C polymorphism with PTB risk in overall or separately in Caucasian population.However,it plays a significant risk factor for predisposing PTB in Asians.Future larger sample and expression studies are needed to validate this association.展开更多
The P2X7 receptor is one of the members of the family of purinoceptors which are ligand-gated membrane ion channels activated by extracellular adenosine 5'-triphosphate. A unique feature of the P2X7 receptor is th...The P2X7 receptor is one of the members of the family of purinoceptors which are ligand-gated membrane ion channels activated by extracellular adenosine 5'-triphosphate. A unique feature of the P2X7 receptor is that its activation can result in the formation of large plasma membrane pores that allow not only the flux of ions but also of hydrophilic molecules of up to 900 Da. Recent studies indicate that P2X7-mediated signaling can trigger apoptotic cell death after ischemia and during the course of certain neurodegenerative disorders. Expression of the P2X7 receptor has been demonstrated in most types of cells in the retina. This purinoceptor mediates the contraction of pericytes and regulates the spatial and temporal dynamics of the vasomotor response through cell-to-cell electrotonic transmission within the microvascular networks. Of potential clinical significance, investigators have found that diabetes markedly boosts the vulnerability of retinal microvessels to the lethal effect of P2X7 receptor activation. This purinergic vasotoxicity may result in reduced retinal blood flow and disrupted vascular function in the diabetic retina. With recent reports indicating an association between P2X7 receptor activation and inflammatory cytokine expression in the retina, this receptor may also exacerbate the development of diabetic retinopathy by a mechanism involving inflammation.展开更多
Background: The aim of this study was to evaluate the clinical potential of new biomarkers such as IL-2, TNF-α, MCP-1, MIP-1β including IFN-γ for the diagnosis of active tuberculosis (TB) disease. Materials and Met...Background: The aim of this study was to evaluate the clinical potential of new biomarkers such as IL-2, TNF-α, MCP-1, MIP-1β including IFN-γ for the diagnosis of active tuberculosis (TB) disease. Materials and Methods: The subjects consisted of 31 patients with active TB disease and 62 patients with non-TB disease. We measured IFN-γ using QuantiFERON-TB Gold In Tube, and IL-2, TNF-α, MCP-1, and MIP-1β using the supernatant from whole blood stimulated with MTB (Mycobacterium tuberculosis)-specific antigens. Results: In the patient group with active TB disease, while the positive response rate of IFN-γ was 74%, that of IL-2 using the supernatant was 61%, TNF-α was 71%, MCP-1 was 81% and MIP-1β was 81%. In the patient group with non-TB disease, while the positive response rate of IFN-γ was 11%, that of IL-2using the supernatant was 32%, TNF-α was 26%, MCP-1 was 23% and MIP-1β was 19%. All biomarker levels of the patients with active TB disease using the supernatant were significantly higher than those of the patients with non-TB disease. While MIP-1β was the most sensitive of all the biomarkers (sensitivity: 80.6%), IFN-γ was the best in terms of specificity (specificity: 87.0%). Conclusions: Several biomarkers, apart from IL-2, showed similar results compared to IFN-γ. The combination of IFN-γ and other new biomarkers may increase the diagnostic accuracy of active TB.展开更多
OBJECTIVE The present study aimed to investigate the relationship between Wnt/β-catenin and Nrf2 signaling pathways,and understanding the mechanisms underlying the process of inflammatory in chronic obstructive pulmo...OBJECTIVE The present study aimed to investigate the relationship between Wnt/β-catenin and Nrf2 signaling pathways,and understanding the mechanisms underlying the process of inflammatory in chronic obstructive pulmonary disease(COPD),which was a serious disease of respiratory system.METHODS We duplicate the emphysema model with porcine pancreatic elastase(PPE)in Nrf2-/-and WT mouse for 21d,and intraperitoneal injection of Li Cl,the activator of Wnt/β-catenin signaling pathway from 14 d to the end.Hematoxylin and eosin(H&E)staining was performed to assess the histopathologic level,and immunohistochemistry(IHC)for Mac-3(the marker of macrophagocyte)and Ly6G(the marker of neutrophil)was used to observe the inflammatory infiltrate,while the levels of Wnt/β-catenin and Nrf2 signaling pathways related proteins heme oxygenase-1(HO-1),NAD(P)H:quinone oxidoreductase 1(NQO1),and the expression of inflammatory cytokine interleukin-6(IL-6)were detected by Western blotting of lung tissues.In vitro,cigarette smoke extract(CSE)-treated normal human bronchial epithelial(NHBE)cells,cell viability was examined by MTT assay,and then we treated recombinant human Wnt3a,si Nrf2 and si Wnt3a to measure the expression of Wnt3a,β-catenin,Nrf2,HO-1,NQO-1,and IL-6.Cellular immunofluorescence staining was employed to identify the nuclear translocation of Nrf2.RESULTS We found that the Li Cl-treated group has markedly decreased the damage of alveolar structure and inflammatory signs than the model group of WT mice rather than Nrf2-/-group.It also seen that Li Cl not only increasedβ-catenin,but it also led to a comparable increase in Nrf2,HO-1,NQO1,and decrease of IL-6 compared with WT model groups but except to Nrf2-/-group in vivo.And it showed that Wnt3atreatment has significantly increased the nuclear translocation of Nrf2 and the expression of HO-1 and NQO1,reduced the IL-6 release,while there has no significance when Nrf2 was blocked in CSE-induced NHBE cells.CONCLUSION Our results demonstrated that Wnt3a/β-catenin significantly balanced oxidative stress and attenuated inflammation reaction by promoting Nrf2 nuclear translocation and activity.展开更多
Objective： To explore the role of interleukin 4（IL-4）, expressions of cyclooxygenase-2 （COX-2） and platelet-derived growth factor （PDGF） in the model of chronic obstructive pulmonary disease （COPD）, in the lu...Objective： To explore the role of interleukin 4（IL-4）, expressions of cyclooxygenase-2 （COX-2） and platelet-derived growth factor （PDGF） in the model of chronic obstructive pulmonary disease （COPD）, in the lungs of rats. Methods： Male Wistar rats were used to build up the model of COPD. Rats were randomly divided into the control group and model group, the IL-4 group and the dexamethasone group. The expressions of COX-2, PDGF-A and PDGF-B in the lung tissue were detected by western blotting and RT-PCR. Results： The expressions of COX-2, PDGF-A and PDGF-B in the model group were increased significantly. Those expressions in the IL-4 and dexamethasone group were notably decreased. Conclusion： IL-4 and dexamethasone could interfere in the establishment of COPD. The expressions of COX-2 and PDGF in the lung tissue of COPD were increased significantly and IL-4 and dexamethasone could decrease those expressions.展开更多
Tuberculosis (TB) is the most common cause of death in infectious diseases; it is estimated that approximately 2 million people per year die of TB. The present available TB vaccine is a live attenuated strain, Mycoba...Tuberculosis (TB) is the most common cause of death in infectious diseases; it is estimated that approximately 2 million people per year die of TB. The present available TB vaccine is a live attenuated strain, Mycobacterium bovis Bacillus Calmette Guérin (BCG). However, it has been shown that BCG has variable protective efficacy, ranging from 0 to 85% in different clinical experiments. 1 Therefore, a new TB vaccine is urgently needed. Many trials have been done to develop the second-generation TB vaccines in recent years; candidates include avirulent, auxotrophic, subunit, DNA, and recombinant vaccines. 2 The outcomes of these vaccines disappointed investigators. Encouragingly, recombinant BCG, which overexpressed the mycobacterial antigen Ag85B, produced an excellent protective response, 3,4 suggesting that a vaccine based on recombinant BCG technique was a potential approach against TB.展开更多
Interleukin-1α and interleukin-1β aggravate neuronal injury by mediating the inf1αmmatory reaction following ischemic/hypoxic brain injury. It remains unclear whether interleukin-1α and interleukin-1β are release...Interleukin-1α and interleukin-1β aggravate neuronal injury by mediating the inf1αmmatory reaction following ischemic/hypoxic brain injury. It remains unclear whether interleukin-1α and interleukin-1β are released by microglia or astrocytes. This study prepared hippocampal slices that were subsequently subjected to oxygen and glucose deprivation. Hematoxylin-eosin staining verified that neurons exhibited hypoxic changes. Results of enzyme-linked immunosorbent assay found that interleukin-1α and interleukin-1β participated in this hypoxic process. Moreover, when hypoxic injury occurred in the hippocampus, the release of interleukin-1α and interleukin-1β was mediated by the P2X4 receptor and P2X7 receptor. Immunofluorescence staining revealed that during ischemia/hypoxia, the P2X4 receptor, P2X7 receptor, interleukin-1α and interleukin-1β expression was detectable in rat hippocampal microglia, but only P2X4 receptor and P2X7 receptor expression was detected in astrocytes. Results suggested that the P2X4 receptor and P2X7 receptor, respectively, mediated interleukin-1α and interleukin-1β released by microglia, resulting in hippocampal ischemic/hypoxic injury. Astrocytes were activated, but did not synthesize or release interleukin-1α and interleukin-1β.展开更多
Previous studies have confirmed that oxidized adenosine triphosphate, a P2X7 receptor antagonist, attenuates lipopolysaccharide-mediated microglial activation and inflammatory expression following neuronal damage in r...Previous studies have confirmed that oxidized adenosine triphosphate, a P2X7 receptor antagonist, attenuates lipopolysaccharide-mediated microglial activation and inflammatory expression following neuronal damage in rat brain. NaCI and temperature may affect the potency of oxidized adenosine triphosphate. Brilliant blue G is a derivative of a widely used food additive and has little toxicity. This study explored the effects of brilliant blue G, a selective P2X7 receptor antagonist, on microglial activation and inflammation. Results demonstrated that brilliant blue G inhibited the release of cydooxygenase-2 and interleukin-6 in BV2 cells. Immunofluorescence displayed that brilliant blue G could suppress lipopolysaccharide-induced microglial activation. This study used RNA interference to block P2X7 receptor expression and found that small interfering RNA also suppressed the release of cyclooxygenase-2 and interleukin-6 in BV2 cells. These results suggested that downregulation of the P2X7 receptor by brilliant blue G was involved in the inhibition of microglial activation and inflammation.展开更多
文摘Background: Tuberculosis (TB) is one of the world’s deadliest infectious diseases. Tumor necrosis factor-Alpha (TNF-α) and Interleukin 8 (IL-8) are involved in the pathogenesis of pulmonary TB (PTB). However, the contribution of polymorphisms of these cytokines to PTB susceptibility needed more investigation across geographic regions and ethnic groups. Purpose: The aim of this study was to investigate the association of the TNF-α-308 G/A and IL-8-251T/A polymorphisms with PTB risk in the Congolese population. Methods: This case-control study included 150 PTB patients and 160 control subjects. Blood samples were collected from all participants and were used for the TNF-α-308 G/A and IL-8-251T/A genotyping by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique. Odds ratios (OR) were calculated to estimate the potential polymorphism associations. A P level of Results: A significant difference was found between PTB patients and controls regarding the TNF-α-308AA genotype (P = 0.035) distribution. Moreover, this genotype was associated with risk to TB (OR = 7.19, 95% CI = 0.85 - 60.65, P = 0.035). The A allele was significantly more frequent in PTB patients than in controls, and was associated with risk to PTB (OR = 1.68, 95% CI = 1.05 - 2.68, P = 0.014). Regarding the IL-8-251T/A gene, TA and AA genotypes were significantly more frequent in PTB patients compared to controls, and were associated with increased risk to PTB (OR = 2.64, 95% CI = 0.97 - 7.18, P = 0.031 and OR = 3.0, 95% CI = 1.13 - 7.98, P = 0.014, respectively). However, the IL-8-251 A allele was not associated to PTB susceptibility (OR = 0.27, 95% CI = 0.15 - 0.44). Conclusion: TNF-α-308G/A and IL-8-251T/A polymorphisms may be associated to PTB susceptibility in the Congolese population, and the AA genotype of both cytokines could be a risk factor.
文摘Objective:To summarize the precise association between pulmonary tuberculosis(PTB) and P2x7 A1513 C gene polymorphism.Methods:PubMed and Google Scholar web-databases were searched for the studies reporting the association of P2x7 A1513 C polymorphism and PTB risk.A meta-analysis was performed for the selected case-control studies and pooled odds ratios(ORs) and 95%confidence intervals(95%CIs) were calculated for all the genetic models.Results:Eleven studies comprising 2 678 controls and 2 113 PTB cases were included in this meta-analysis.We observed overall no significant risk in all the five genetic models.When stratified population by the ethnicity,Caucasian population failed to show any risk of PTB in all the genetics models.In Asian ethnicity,variant allele(C vs.A:P=0.001;QR=1.375,95%CI=1.159-1.632) and heterozygous genotype(AC vs.AA:P=0.001;OR=1.570,95%CI=1.269-1.944) demonstrated significant increased risk of PTB.Likewise,recessive genetic model(CC+AC vs.AA:P=0.001;OR=1.540,95%CI= 1.255-1.890) also demonstrated increased risk of PTB in Asians.Conclusions:Our meta-analysis did not suggest the association of P2x7 A1513 C polymorphism with PTB risk in overall or separately in Caucasian population.However,it plays a significant risk factor for predisposing PTB in Asians.Future larger sample and expression studies are needed to validate this association.
文摘The P2X7 receptor is one of the members of the family of purinoceptors which are ligand-gated membrane ion channels activated by extracellular adenosine 5'-triphosphate. A unique feature of the P2X7 receptor is that its activation can result in the formation of large plasma membrane pores that allow not only the flux of ions but also of hydrophilic molecules of up to 900 Da. Recent studies indicate that P2X7-mediated signaling can trigger apoptotic cell death after ischemia and during the course of certain neurodegenerative disorders. Expression of the P2X7 receptor has been demonstrated in most types of cells in the retina. This purinoceptor mediates the contraction of pericytes and regulates the spatial and temporal dynamics of the vasomotor response through cell-to-cell electrotonic transmission within the microvascular networks. Of potential clinical significance, investigators have found that diabetes markedly boosts the vulnerability of retinal microvessels to the lethal effect of P2X7 receptor activation. This purinergic vasotoxicity may result in reduced retinal blood flow and disrupted vascular function in the diabetic retina. With recent reports indicating an association between P2X7 receptor activation and inflammatory cytokine expression in the retina, this receptor may also exacerbate the development of diabetic retinopathy by a mechanism involving inflammation.
文摘Background: The aim of this study was to evaluate the clinical potential of new biomarkers such as IL-2, TNF-α, MCP-1, MIP-1β including IFN-γ for the diagnosis of active tuberculosis (TB) disease. Materials and Methods: The subjects consisted of 31 patients with active TB disease and 62 patients with non-TB disease. We measured IFN-γ using QuantiFERON-TB Gold In Tube, and IL-2, TNF-α, MCP-1, and MIP-1β using the supernatant from whole blood stimulated with MTB (Mycobacterium tuberculosis)-specific antigens. Results: In the patient group with active TB disease, while the positive response rate of IFN-γ was 74%, that of IL-2 using the supernatant was 61%, TNF-α was 71%, MCP-1 was 81% and MIP-1β was 81%. In the patient group with non-TB disease, while the positive response rate of IFN-γ was 11%, that of IL-2using the supernatant was 32%, TNF-α was 26%, MCP-1 was 23% and MIP-1β was 19%. All biomarker levels of the patients with active TB disease using the supernatant were significantly higher than those of the patients with non-TB disease. While MIP-1β was the most sensitive of all the biomarkers (sensitivity: 80.6%), IFN-γ was the best in terms of specificity (specificity: 87.0%). Conclusions: Several biomarkers, apart from IL-2, showed similar results compared to IFN-γ. The combination of IFN-γ and other new biomarkers may increase the diagnostic accuracy of active TB.
基金The project supported by National Natural Science Foundation of China(81274172,81473267,30801535,81470003)
文摘OBJECTIVE The present study aimed to investigate the relationship between Wnt/β-catenin and Nrf2 signaling pathways,and understanding the mechanisms underlying the process of inflammatory in chronic obstructive pulmonary disease(COPD),which was a serious disease of respiratory system.METHODS We duplicate the emphysema model with porcine pancreatic elastase(PPE)in Nrf2-/-and WT mouse for 21d,and intraperitoneal injection of Li Cl,the activator of Wnt/β-catenin signaling pathway from 14 d to the end.Hematoxylin and eosin(H&E)staining was performed to assess the histopathologic level,and immunohistochemistry(IHC)for Mac-3(the marker of macrophagocyte)and Ly6G(the marker of neutrophil)was used to observe the inflammatory infiltrate,while the levels of Wnt/β-catenin and Nrf2 signaling pathways related proteins heme oxygenase-1(HO-1),NAD(P)H:quinone oxidoreductase 1(NQO1),and the expression of inflammatory cytokine interleukin-6(IL-6)were detected by Western blotting of lung tissues.In vitro,cigarette smoke extract(CSE)-treated normal human bronchial epithelial(NHBE)cells,cell viability was examined by MTT assay,and then we treated recombinant human Wnt3a,si Nrf2 and si Wnt3a to measure the expression of Wnt3a,β-catenin,Nrf2,HO-1,NQO-1,and IL-6.Cellular immunofluorescence staining was employed to identify the nuclear translocation of Nrf2.RESULTS We found that the Li Cl-treated group has markedly decreased the damage of alveolar structure and inflammatory signs than the model group of WT mice rather than Nrf2-/-group.It also seen that Li Cl not only increasedβ-catenin,but it also led to a comparable increase in Nrf2,HO-1,NQO1,and decrease of IL-6 compared with WT model groups but except to Nrf2-/-group in vivo.And it showed that Wnt3atreatment has significantly increased the nuclear translocation of Nrf2 and the expression of HO-1 and NQO1,reduced the IL-6 release,while there has no significance when Nrf2 was blocked in CSE-induced NHBE cells.CONCLUSION Our results demonstrated that Wnt3a/β-catenin significantly balanced oxidative stress and attenuated inflammation reaction by promoting Nrf2 nuclear translocation and activity.
文摘Objective： To explore the role of interleukin 4（IL-4）, expressions of cyclooxygenase-2 （COX-2） and platelet-derived growth factor （PDGF） in the model of chronic obstructive pulmonary disease （COPD）, in the lungs of rats. Methods： Male Wistar rats were used to build up the model of COPD. Rats were randomly divided into the control group and model group, the IL-4 group and the dexamethasone group. The expressions of COX-2, PDGF-A and PDGF-B in the lung tissue were detected by western blotting and RT-PCR. Results： The expressions of COX-2, PDGF-A and PDGF-B in the model group were increased significantly. Those expressions in the IL-4 and dexamethasone group were notably decreased. Conclusion： IL-4 and dexamethasone could interfere in the establishment of COPD. The expressions of COX-2 and PDGF in the lung tissue of COPD were increased significantly and IL-4 and dexamethasone could decrease those expressions.
文摘Tuberculosis (TB) is the most common cause of death in infectious diseases; it is estimated that approximately 2 million people per year die of TB. The present available TB vaccine is a live attenuated strain, Mycobacterium bovis Bacillus Calmette Guérin (BCG). However, it has been shown that BCG has variable protective efficacy, ranging from 0 to 85% in different clinical experiments. 1 Therefore, a new TB vaccine is urgently needed. Many trials have been done to develop the second-generation TB vaccines in recent years; candidates include avirulent, auxotrophic, subunit, DNA, and recombinant vaccines. 2 The outcomes of these vaccines disappointed investigators. Encouragingly, recombinant BCG, which overexpressed the mycobacterial antigen Ag85B, produced an excellent protective response, 3,4 suggesting that a vaccine based on recombinant BCG technique was a potential approach against TB.
基金supported by the Natural Science Foundation of Guangdong Province,No.S2011010004096
文摘Interleukin-1α and interleukin-1β aggravate neuronal injury by mediating the inf1αmmatory reaction following ischemic/hypoxic brain injury. It remains unclear whether interleukin-1α and interleukin-1β are released by microglia or astrocytes. This study prepared hippocampal slices that were subsequently subjected to oxygen and glucose deprivation. Hematoxylin-eosin staining verified that neurons exhibited hypoxic changes. Results of enzyme-linked immunosorbent assay found that interleukin-1α and interleukin-1β participated in this hypoxic process. Moreover, when hypoxic injury occurred in the hippocampus, the release of interleukin-1α and interleukin-1β was mediated by the P2X4 receptor and P2X7 receptor. Immunofluorescence staining revealed that during ischemia/hypoxia, the P2X4 receptor, P2X7 receptor, interleukin-1α and interleukin-1β expression was detectable in rat hippocampal microglia, but only P2X4 receptor and P2X7 receptor expression was detected in astrocytes. Results suggested that the P2X4 receptor and P2X7 receptor, respectively, mediated interleukin-1α and interleukin-1β released by microglia, resulting in hippocampal ischemic/hypoxic injury. Astrocytes were activated, but did not synthesize or release interleukin-1α and interleukin-1β.
基金supported by the National Natural Science Foundation of China, No. 81072242the Excellent Supervisor & Yat-Sen Creative Talent Development Program of Sun Yat-sen University
文摘Previous studies have confirmed that oxidized adenosine triphosphate, a P2X7 receptor antagonist, attenuates lipopolysaccharide-mediated microglial activation and inflammatory expression following neuronal damage in rat brain. NaCI and temperature may affect the potency of oxidized adenosine triphosphate. Brilliant blue G is a derivative of a widely used food additive and has little toxicity. This study explored the effects of brilliant blue G, a selective P2X7 receptor antagonist, on microglial activation and inflammation. Results demonstrated that brilliant blue G inhibited the release of cydooxygenase-2 and interleukin-6 in BV2 cells. Immunofluorescence displayed that brilliant blue G could suppress lipopolysaccharide-induced microglial activation. This study used RNA interference to block P2X7 receptor expression and found that small interfering RNA also suppressed the release of cyclooxygenase-2 and interleukin-6 in BV2 cells. These results suggested that downregulation of the P2X7 receptor by brilliant blue G was involved in the inhibition of microglial activation and inflammation.
