astrocyte星形胶质细胞.ppt
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星形胶质细胞
（2）递质代谢。星形胶质细胞是谷氨酸（Glu）和γ-氨基丁酸（GABA）代谢的场所，谷氨酸和GABA被神经 元释放后都可以被星形胶质细胞所摄取，经酶催化后可转变为谷氨酰胺（Gln），Gln是可以分别被谷氨酸能和 GABA能神经元利用的前体，分别可以被转变为谷氨酸和GABA。另外，围绕突触的星形胶质细胞可以构成一道屏障， 避免递质从突触间隙扩散出去。
星形胶质细胞具有许多突起，伸展充填在神经细胞的胞体及其突起之间，起支持和分隔神经细胞的作用，并 参与了血脑屏障的形成。由于星形胶质细胞能产生和分泌某些神经递质以及表达某些神经递质受体，可对一些神 经活性物质产生反应。另外，星形胶质细胞能对外源性化合物进行生物转化，并可帮助调节神经元周围的离子微 环境。外源性化学物质或外伤损伤中枢神经系统后，损伤区域星形胶质细胞通过增生可形成胶质“瘢痕”。这种 增殖多伴随着胶质纤维酸性蛋白（ glial fibrillary acidic protein，GFAP）的表达增加。因此组织中GFAP 升高是中枢神经系统对损伤作出反应的一个标志性信号。
星形胶质细胞比脑内其他任何类型的细胞具有更广泛的缝隙连接，由此使得星形胶质细胞类似于合胞体样结 构。这种缝隙连接的功能为：加强相邻细胞的连接；细胞通讯，其方式为离子偶联以及代谢物偶联。离子偶联即 电偶联，可使细胞形成同步活动。而代谢偶联则能使单糖、氨基酸、核苷酸、维生素以及激素和其他一些低分子 物质自由通过缝隙连接。
（3）营养和保护作用。在神经发育中的作用，星形胶质细胞的终足几乎包被脑毛细血管80%以上的面积，而 其与脑毛细血管内皮细胞之间的紧密连接可能是形成血脑屏障的基础，并从血液中摄取营养物质供应神经元。在 胚胎发育初期放射状胶质细胞可以引导神经细胞迁移。在中枢神经系统受损后，星形胶质细胞进行有丝分裂，容 易形成胶质瘢痕。
星形胶质细胞具有许多突起，伸展充填在神经细胞的胞体及其突起之间，起支持和分隔神经细胞的作用，并 参与了血脑屏障的形成。由于星形胶质细胞能产生和分泌某些神经递质以及表达某些神经递质受体，可对一些神 经活性物质产生反应。另外，星形胶质细胞能对外源性化合物进行生物转化，并可帮助调节神经元周围的离子微 环境。外源性化学物质或外伤损伤中枢神经系统后，损伤区域星形胶质细胞通过增生可形成胶质“瘢痕”。这种 增殖多伴随着胶质纤维酸性蛋白（ glial fibrillary acidic protein，GFAP）的表达增加。因此组织中GFAP 升高是中枢神经系统对损伤作出反应的一个标志性信号。
星形胶质细胞比脑内其他任何类型的细胞具有更广泛的缝隙连接，由此使得星形胶质细胞类似于合胞体样结 构。这种缝隙连接的功能为：加强相邻细胞的连接；细胞通讯，其方式为离子偶联以及代谢物偶联。离子偶联即 电偶联，可使细胞形成同步活动。而代谢偶联则能使单糖、氨基酸、核苷酸、维生素以及激素和其他一些低分子 物质自由通过缝隙连接。
（3）营养和保护作用。在神经发育中的作用，星形胶质细胞的终足几乎包被脑毛细血管80%以上的面积，而 其与脑毛细血管内皮细胞之间的紧密连接可能是形成血脑屏障的基础，并从血液中摄取营养物质供应神经元。在 胚胎发育初期放射状胶质细胞可以引导神经细胞迁移。在中枢神经系统受损后，星形胶质细胞进行有丝分裂，容 易形成胶质瘢痕。
astrocyte(星形胶质细胞)
完整ppt课件
3
4 Interestingly, lack of TNF-α signal transduction reduced UCB-induced cell death for short periods of incubation, in contrast, inhibition of IL-1 β cascade produced a sustained blockade of astrocyte injury by UCB.
Astrocyte Reactivity to Unconjugated Bilirubin Requires TNF-α and IL-1β Receptor Signaling
Pathways
GLIA 59:14–25 (2011) SCI(2010)：5.19
周康康 2012-7-2
完整ppt课件
3 Cell Treatment ：50μM UCB plus 100μM human serum albumin (HSA) (UCB to HSA molar ratio of 0.5), from15 min to 24 h, at 370C.
4 Western Blot ：The protein expression of TNFR1, TNFR2, and IL-1R1were determined by Western blot analysis.
完整ppt课件
5
5 Measurement of Cytokine Release ：TNF-α, IL-1β, and IL-6 with specific DuoSetR ELISA Development kits.
6 Detection of NF-κB Activation — immunofluorescence detection ：rabbit anti-p65 NF- κB subunit antibody (1:200) as the primary antibodies, a FITC-labeled goat anti-rabbit antibody (1:160) as the secondary antibodieastrocytes to UCB increased the expression of both TNF- α receptor TNFR1 and IL-1 β receptor IL-1R1, but not TNFR2, as well as their activation, observed by augmented binding of receptors’ molecular adaptors, TRAF2 and TRAF6, respectively.
astrocyte(星形胶质细胞)
Astrocyte Reactivity to Unconjugated Bilirubin Requires TNF-α and IL-1β Receptor Signaling
Pathways
GLIA 59:14–25 (2011) SCI(2010)：5.19
周康康 2012-7-2
1
Summary
5
5 Measurement of Cytokine Release ：TNF-α, IL-1β, and IL-6 with specific DuoSetR ELISA Development kits.
6 Detection of NF-κB Activation — immunofluorescence detection ：rabbit anti-p65 NF- κB subunit antibody (1:200) as the primary antibodies, a FITC-labeled goat anti-rabbit antibody (1:160) as the secondary antibodies.
3 Cell Treatment ：50μM UCB plus 100μM human serum albumin (HSA) (UCB to HSA molar ratio of 0.5), from15 min to 24 h, at 370C.
4 Western Blot ：The protein expression of TNFR1, TNFR2, and IL-1R1were determined by Western blot analysis.
6
Results
1 UCB Increases the Protein Content of TNFR1 and IL-1R1, but not of TNFR2, and Induces Their Engagement.
Pathways
GLIA 59:14–25 (2011) SCI(2010)：5.19
周康康 2012-7-2
1
Summary
5
5 Measurement of Cytokine Release ：TNF-α, IL-1β, and IL-6 with specific DuoSetR ELISA Development kits.
6 Detection of NF-κB Activation — immunofluorescence detection ：rabbit anti-p65 NF- κB subunit antibody (1:200) as the primary antibodies, a FITC-labeled goat anti-rabbit antibody (1:160) as the secondary antibodies.
3 Cell Treatment ：50μM UCB plus 100μM human serum albumin (HSA) (UCB to HSA molar ratio of 0.5), from15 min to 24 h, at 370C.
4 Western Blot ：The protein expression of TNFR1, TNFR2, and IL-1R1were determined by Western blot analysis.
6
Results
1 UCB Increases the Protein Content of TNFR1 and IL-1R1, but not of TNFR2, and Induces Their Engagement.
astrocyte(星形胶质细胞)
3
4 Interestingly, lack of TNF-α signal transduction reduced UCB-induced cell death for short periods of incubation, in contrast, inhibition of IL-1 β cascade produced a sustained blockade of astrocyte injury by UCB.
Astrocyte Reactivity to Unconjugated Bilirubin Requires TNF-α and IL-1β Receptor Signaling
Pathways
GLIA 59:14–25 (2011) SCI(2010)：5.19
周康康 2012-75 Measurement of Cytokine Release ：TNF-α, IL-1β, and IL-6 with specific DuoSetR ELISA Development kits.
6 Detection of NF-κB Activation — immunofluorescence detection ：rabbit anti-p65 NF- κB subunit antibody (1:200) as the primary antibodies, a FITC-labeled goat anti-rabbit antibody (1:160) as the secondary antibodies.
3 Cell Treatment ：50μM UCB plus 100μM human serum albumin (HSA) (UCB to HSA molar ratio of 0.5), from15 min to 24 h, at 370C.
4 Interestingly, lack of TNF-α signal transduction reduced UCB-induced cell death for short periods of incubation, in contrast, inhibition of IL-1 β cascade produced a sustained blockade of astrocyte injury by UCB.
Astrocyte Reactivity to Unconjugated Bilirubin Requires TNF-α and IL-1β Receptor Signaling
Pathways
GLIA 59:14–25 (2011) SCI(2010)：5.19
周康康 2012-75 Measurement of Cytokine Release ：TNF-α, IL-1β, and IL-6 with specific DuoSetR ELISA Development kits.
6 Detection of NF-κB Activation — immunofluorescence detection ：rabbit anti-p65 NF- κB subunit antibody (1:200) as the primary antibodies, a FITC-labeled goat anti-rabbit antibody (1:160) as the secondary antibodies.
3 Cell Treatment ：50μM UCB plus 100μM human serum albumin (HSA) (UCB to HSA molar ratio of 0.5), from15 min to 24 h, at 370C.
astrocyte(星形胶质细胞)
astrocyte(星形胶质细胞)
Summary
1 We have reported that tumor necrosis factor (TNF)-α and interleukin (IL)-1β are produced by cultured neurons and mainly by glial cells exposed to unconjugated bilirubin (UCB). The effects of these cytokines are mediated by cell surface receptors through a nuclear factor (NF)-κB-dependent pathway that we have showed to be activated by UCB.
3 Silencing of TNFR1, using siRNA technology, or blockade of IL-1 β cascade, using its endogenous antagonist, IL-1 receptor antagonist (IL-1ra), prevented UCB-induced cytokine release and NF-κ B activation.
5
5 Measurement of Cytokine Release ：TNF-α, IL-1β, and IL-6 with specific DuoSetR ELISA Development kits.
6 Detection of NF-κB Activation — immunofluorescence detection ：rabbit anti-p65 NF- κB subunit antibody (1:200) as the primary antibodies, a FITC-labeled goat anti-rabbit antibody (1:160) as the secondary antibodies.
Summary
1 We have reported that tumor necrosis factor (TNF)-α and interleukin (IL)-1β are produced by cultured neurons and mainly by glial cells exposed to unconjugated bilirubin (UCB). The effects of these cytokines are mediated by cell surface receptors through a nuclear factor (NF)-κB-dependent pathway that we have showed to be activated by UCB.
3 Silencing of TNFR1, using siRNA technology, or blockade of IL-1 β cascade, using its endogenous antagonist, IL-1 receptor antagonist (IL-1ra), prevented UCB-induced cytokine release and NF-κ B activation.
5
5 Measurement of Cytokine Release ：TNF-α, IL-1β, and IL-6 with specific DuoSetR ELISA Development kits.
6 Detection of NF-κB Activation — immunofluorescence detection ：rabbit anti-p65 NF- κB subunit antibody (1:200) as the primary antibodies, a FITC-labeled goat anti-rabbit antibody (1:160) as the secondary antibodies.
astrocyte(星形胶质细胞)
3
4 Interestingly, lack of TNF-α signal transduction reduced UCB-induced cell death for short periods of incubation, in contrast, inhibition of IL-1 β cascade produced a sustained blockade of astrocyte injury by UCB.
14
15
16
4 Silencing of TNFR1 and Suppression Activation of NF-κB.
17
18
19
5 Silencing of TNFR1 and Suppression of IL-1R1 Activity Modulates UCB-Induced Cytotoxicity.
5
5 Measurement of Cytokine Release ：TNF-α, IL-1β, and IL-6 with specific DuoSetR ELISA Development kits.
6 Detection of NF-κB Activation — immunofluorescence detection ：rabbit anti-p65 NF- κB subunit antibody (1:200) as the primary antibodies, a FITC-labeled goat anti-rabbit antibody (1:160) as the secondary antibodies. 7 Evaluation of Cell Death — LDH Astrocytes were then identified in fixed cells by an antibody directed against GFAP.（神经胶质原纤维酸性蛋白） To identify the total number of cells, astroglial nuclei were stained with Hoechst dye 33258.（烟酸己可碱 — DNA染料）
《星形胶质细胞》课件
星形胶质细胞的分类
• 纤维型星形胶质细胞 • 间质型星形胶质细胞 • 脂质型星形胶质细胞 • 守望星形胶质细胞
星形胶质细胞在疾病中的作用
星形胶质细胞在多种神经系统疾病中发挥重要的作用，如帕金森病、阿尔茨海默病等。通过调节细胞代谢、炎 症反应等，星形胶质细胞对病理过程产生重要影响。
结论和要点
• 星形胶质细胞是中枢神经系统的重要组成部分，发挥多种重要功能。 • 星形胶质细胞与神经元密切联系，形成复杂的神经-胶质网络。 • 胶质细胞在神经系统疾病中扮演重要角色，对病理过程产生重要影响。
《星形胶质细胞》PPT课 件
星形胶质细胞是中枢神经系统中的一种主要细胞类型，其形状独特，拥有重 要的结构和功能。
星形胶质细胞的定义
星形胶质细胞是中枢神经系统中的一种胶质细胞类型，其形态似星星状，其 名称即由此得来。
星形胶质细胞的结构
• 星形胶质细胞具有细长的纤维突起，可与其他细胞进行联系。 • 细胞体中含有丰富的胞质，提供细胞的能量和营养。 • 胞质内含有星形的线粒体，用于细胞的能量代谢。
星形胶质细胞的功能
• 星形胶质细胞参与了维持神经系统稳定的功能，形成了神经递质的代 谢循环。
• 胶质细胞提供营养和氧气给周围的神经细胞，有助于维持神神经系统的正常 运作。
星形胶质细胞与神经元的关系
星形胶质细胞与神经元紧密联系，形成了复杂的神经-胶质网络。胶质细胞提 供支持和保护，同时也与神经元进行信息传递。
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5 Together, our data show that inflammatory pathways are activated during in vitro exposure of rat astrocytes to UCB. This supports the concept that inflammatory pathways play a role in brain damage by UCB, and that they may represent important pharmacological targets.
3
4 Interestingly, lack of TNF-α signal transduction reduced UCB-induced cell death for short periods of incubation, in contrast, inhibition of IL-1 β cascade produced a sustained blockade of astrocyte injury by UCB.
5
5 Measurement of Cytokine Release ：TNF-α, IL-1β, and IL-6 with specific DuoSetR ELISA Development kits.
6 Detection of NF-κB Activation — immunofluorescence detection ：rabbit anti-p65 NF- κB subunit antibody (1:200) as the primary antibodies, a FITC-labeled goat anti-rabbit antibody (1:160) as the secondary antibodies.
3 Silencing of TNFR1, using siRNA technology, or blockade of IL-1 β cascade, using its endogenous antagonist, IL-1 receptor antagonist (IL-1ra), prevented UCB-induced cytokine release and NF-κ B activation.
4
Materials and methods
1 Primary Culture of Astrocytes ：2-day-old Wistar rats
2 Transient Transfection ：three different doublestrand ed rat TNFR1 small interfering (si)RNAs (30 n M), scrambled siRNA (negative control) or the absence of siRNA (mock control).
3 Cell Treatment ：50μM UCB plus 100μM human serum albumin (HSA) (UCB to HSA molar ratio of 0.5), from15 min to 24 h, at 370C.
4 Western Blot ：The protein expression of TNFR1, TNFR2, and IL-1R1were determined by Western blot analysis.
7 Evaluation of Cell Death — LDH Astrocytes were then identified in fixed cells by an antibody directed against GFAP.（神经胶质原纤维酸性蛋白） To identify the total number of cells, astroglial nuclei were stained with Hoechst dye 33258.（烟酸己可碱 — DNA染料）
2
2 Exposure of astrocytes to UCB increased the expression of both TNF- α receptor TNFR1 and IL-1 β receptor IL-1R1, but not TNFR2, as well as their activation, observed by augmented binding of receptors’ molecular adaptors, TRAF2 and TRAF6, respectively.
6
Results
1 UCB Increases the Protein Content of TNFR1 and IL-1R1, but not of TNFR2, and Induces Their Engagement.
1 We have reported that tumor necrosis factor (TNF)-α and interleukin (IL)-1β are produced by cultured neurons and mainly by glial cells exposed to unconjugated bilirubin (UCB). The effects of these receptors through a nuclear factor (NF)-κB-dependent pathway that we have showed to be activated by UCB.
Astrocyte Reactivity to Unconjugated Bilirubin Requires TNF-α and IL-1β Receptor Signaling
Pathways
GLIA 59:14–25 (2019) SCI(2019)：5.19
周康康 2019-7-2
1
Summary
3
4 Interestingly, lack of TNF-α signal transduction reduced UCB-induced cell death for short periods of incubation, in contrast, inhibition of IL-1 β cascade produced a sustained blockade of astrocyte injury by UCB.
5
5 Measurement of Cytokine Release ：TNF-α, IL-1β, and IL-6 with specific DuoSetR ELISA Development kits.
6 Detection of NF-κB Activation — immunofluorescence detection ：rabbit anti-p65 NF- κB subunit antibody (1:200) as the primary antibodies, a FITC-labeled goat anti-rabbit antibody (1:160) as the secondary antibodies.
3 Silencing of TNFR1, using siRNA technology, or blockade of IL-1 β cascade, using its endogenous antagonist, IL-1 receptor antagonist (IL-1ra), prevented UCB-induced cytokine release and NF-κ B activation.
4
Materials and methods
1 Primary Culture of Astrocytes ：2-day-old Wistar rats
2 Transient Transfection ：three different doublestrand ed rat TNFR1 small interfering (si)RNAs (30 n M), scrambled siRNA (negative control) or the absence of siRNA (mock control).
3 Cell Treatment ：50μM UCB plus 100μM human serum albumin (HSA) (UCB to HSA molar ratio of 0.5), from15 min to 24 h, at 370C.
4 Western Blot ：The protein expression of TNFR1, TNFR2, and IL-1R1were determined by Western blot analysis.
7 Evaluation of Cell Death — LDH Astrocytes were then identified in fixed cells by an antibody directed against GFAP.（神经胶质原纤维酸性蛋白） To identify the total number of cells, astroglial nuclei were stained with Hoechst dye 33258.（烟酸己可碱 — DNA染料）
2
2 Exposure of astrocytes to UCB increased the expression of both TNF- α receptor TNFR1 and IL-1 β receptor IL-1R1, but not TNFR2, as well as their activation, observed by augmented binding of receptors’ molecular adaptors, TRAF2 and TRAF6, respectively.
6
Results
1 UCB Increases the Protein Content of TNFR1 and IL-1R1, but not of TNFR2, and Induces Their Engagement.
1 We have reported that tumor necrosis factor (TNF)-α and interleukin (IL)-1β are produced by cultured neurons and mainly by glial cells exposed to unconjugated bilirubin (UCB). The effects of these receptors through a nuclear factor (NF)-κB-dependent pathway that we have showed to be activated by UCB.
Astrocyte Reactivity to Unconjugated Bilirubin Requires TNF-α and IL-1β Receptor Signaling
Pathways
GLIA 59:14–25 (2019) SCI(2019)：5.19
周康康 2019-7-2
1
Summary