Department of Rehabilitation Medicine and Physical Therapy, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 400010, P.R. China.
Department of Rehabilitation Medicine, Hainan General Hospital, Haikou, Hainan 570311, P.R. China.
Mol Med Rep. 2018 Jan;17(1):2026-2032. doi: 10.3892/mmr.2017.8026. Epub 2017 Nov 10.
Gamboge is the dry resin secreted by Garcinia hanburyi Hook.f, with the function of promoting blood circulation, detoxification, hemostasis and killing insects, used for the treatment of cancer, brain edema and other diseases. Gambogic acid is the main effective constituent of Gamboge. The present study investigated the protective effects of gambogic acid on spinal cord injury (SCI) and its anti‑inflammatory mechanism in an SCI model in vivo. Basso, Beattie and Bresnahan (BBB) testing was used to detect the protective effects of gambogic acid on nerve function of SCI rats. The water content of the spinal cord was used to analyze the protective effects of gambogic acid on the damage of SCI. Treatment with gambogic acid effectively improved BBB scores and inhibited water content of the spinal cord in SCI rats. Also, gambogic acid significantly reduced inflammatory cytokines levels of [tumor necrosis factor‑α, interleukin (IL)‑6, IL‑12 and IL‑1β] and oxidative stress (malondialdehyde, superoxide dismutase, glutathione and glutathione‑peroxidase) factors, and suppressed receptor activator of nuclear factor κB ligand, phosphorylated p38 protein expression and toll‑like receptor 4/nuclear factor‑κB pathway activation, and increased phosphatidylinositol 3‑kinase/protein kinase B (Akt) pathway activation in SCI rats. These results provide evidence that gambogic acid inhibits SCI and inflammation through suppressing the p38 and Akt signaling pathways.
藤黄是藤黄属植物藤黄分泌的干燥树脂，具有活血、解毒、止血、杀虫的作用，用于治疗癌症、脑水肿等疾病。藤黄酸是藤黄的主要有效成分。本研究在体内脊髓损伤（SCI）模型中探讨了藤黄酸对脊髓损伤的保护作用及其抗炎机制。Basso、Beattie 和 Bresnahan（BBB）测试用于检测藤黄酸对 SCI 大鼠神经功能的保护作用。通过分析脊髓含水量来评估藤黄酸对 SCI 损伤的保护作用。藤黄酸治疗可有效提高 BBB 评分并抑制 SCI 大鼠脊髓含水量。此外，藤黄酸还显著降低了肿瘤坏死因子-α、白细胞介素（IL）-6、IL-12 和 IL-1β 等炎症细胞因子水平以及氧化应激（丙二醛、超氧化物歧化酶、谷胱甘肽和谷胱甘肽过氧化物酶）因子水平，并抑制了核因子 κB 受体激活物配体、磷酸化 p38 蛋白表达和 Toll 样受体 4/核因子-κB 通路的激活，同时增加了 SCI 大鼠中磷酸肌醇 3-激酶/蛋白激酶 B（Akt）通路的激活。这些结果为藤黄酸通过抑制 p38 和 Akt 信号通路抑制 SCI 和炎症提供了证据。
