Abstract：
UNASSIGNED: Apoptosis, inflammation, and the extracellular matrix (ECM) synthesis and catabolism are compromised with intervertebral disc degeneration (IDD). Ginkgetin (GK) has been demonstrated to alleviate several diseases; however, its effect on IDD remains unknown.
UNASSIGNED: The nucleus pulposus cells (NPCs) were stimulated with interleukin (IL)-1β to construct the IDD models in vitro. Rats were used for the construction of the IDD models in vivo via the fibrous ring puncture method. The effect and mechanism of GK on IDD were determined by cell counting kit-8 (CCK-8), flow cytometry, western blot, real-time quantitative polymerase chain reaction (RT-qPCR), enzyme‑linked immunosorbent assay (ELISA), hematoxylin and eosin (HE) and safranine O staining, and immunohistochemistry (IHC) assays, respectively.
UNASSIGNED: GK increased the cell viability and upregulated the expressions of anti-apoptosis and ECM synthesis markers in NPCs treated with IL-1β. GK also decreased apoptosis rate, and downregulated the expressions of proteins related to pro-apoptosis, ECM catabolism, and inflammation in vitro. Mechanically, GK reduced the expression of nucleotide binding oligomeric domain like receptor protein 3 (NLRP3) inflammasome-related proteins. Overexpression of NLRP3 reversed the effect of GK on the proliferation, apoptosis, inflammation, and ECM degradation in IL-1β-induced NPCs. Moreover, GK attenuated the pathological manifestations, inflammation, ECM degradation, and NLRP3 inflammasome expression in IDD rats.
UNASSIGNED: GK suppressed apoptosis, inflammation, and ECM degradation to alleviate IDD via the inactivation of NLRP3 inflammasome.
UNASSIGNED: The nucleus pulposus cells (NPCs) were stimulated with interleukin (IL)-1β to construct the IDD models in vitro. Rats were used for the construction of the IDD models in vivo via the fibrous ring puncture method. The effect and mechanism of GK on IDD were determined by cell counting kit-8 (CCK-8), flow cytometry, western blot, real-time quantitative polymerase chain reaction (RT-qPCR), enzyme‑linked immunosorbent assay (ELISA), hematoxylin and eosin (HE) and safranine O staining, and immunohistochemistry (IHC) assays, respectively.
UNASSIGNED: GK increased the cell viability and upregulated the expressions of anti-apoptosis and ECM synthesis markers in NPCs treated with IL-1β. GK also decreased apoptosis rate, and downregulated the expressions of proteins related to pro-apoptosis, ECM catabolism, and inflammation in vitro. Mechanically, GK reduced the expression of nucleotide binding oligomeric domain like receptor protein 3 (NLRP3) inflammasome-related proteins. Overexpression of NLRP3 reversed the effect of GK on the proliferation, apoptosis, inflammation, and ECM degradation in IL-1β-induced NPCs. Moreover, GK attenuated the pathological manifestations, inflammation, ECM degradation, and NLRP3 inflammasome expression in IDD rats.
UNASSIGNED: GK suppressed apoptosis, inflammation, and ECM degradation to alleviate IDD via the inactivation of NLRP3 inflammasome.
摘要：
■细胞凋亡，炎症,椎间盘退变（IDD）会损害细胞外基质（ECM）的合成和分解代谢。银杏素（GK）已被证明可以缓解多种疾病；然而，它对IDD的影响仍然未知。
■用白细胞介素（IL）-1β刺激髓核细胞（NPCs），以构建体外IDD模型。通过纤维环穿刺方法将大鼠用于体内IDD模型的构建。细胞计数试剂盒-8(CCK-8)检测GK对IDD的作用及机制,流式细胞术,westernblot,实时定量聚合酶链反应（RT-qPCR），酶联免疫吸附测定（ELISA），苏木精和伊红（HE）和藏红O染色，和免疫组织化学（IHC）测定，分别。
■GK增加了IL-1β处理的NPCs的细胞活力，并上调了抗凋亡和ECM合成标志物的表达。GK也降低了细胞凋亡率，下调促凋亡相关蛋白的表达，ECM分解代谢，和体外炎症。机械上,GK降低核苷酸结合寡聚结构域样受体蛋白3(NLRP3)炎性体相关蛋白的表达。过表达NLRP3逆转了GK对细胞增殖的影响,凋亡，炎症,IL-1β诱导的NPC中的ECM降解。此外，GK减弱了病理表现，炎症,ECM降解，和NLRP3炎性体在IDD大鼠中的表达。
■GK抑制细胞凋亡，炎症,和ECM降解通过NLRP3炎性体的失活来减轻IDD。
■用白细胞介素（IL）-1β刺激髓核细胞（NPCs），以构建体外IDD模型。通过纤维环穿刺方法将大鼠用于体内IDD模型的构建。细胞计数试剂盒-8(CCK-8)检测GK对IDD的作用及机制,流式细胞术,westernblot,实时定量聚合酶链反应（RT-qPCR），酶联免疫吸附测定（ELISA），苏木精和伊红（HE）和藏红O染色，和免疫组织化学（IHC）测定，分别。
■GK增加了IL-1β处理的NPCs的细胞活力，并上调了抗凋亡和ECM合成标志物的表达。GK也降低了细胞凋亡率，下调促凋亡相关蛋白的表达，ECM分解代谢，和体外炎症。机械上,GK降低核苷酸结合寡聚结构域样受体蛋白3(NLRP3)炎性体相关蛋白的表达。过表达NLRP3逆转了GK对细胞增殖的影响,凋亡，炎症,IL-1β诱导的NPC中的ECM降解。此外，GK减弱了病理表现，炎症,ECM降解，和NLRP3炎性体在IDD大鼠中的表达。
■GK抑制细胞凋亡，炎症,和ECM降解通过NLRP3炎性体的失活来减轻IDD。
