Tanshinone IIA attenuates the inflammatory response and apoptosis after traumatic injury of the spinal cord in adult rats.
Tanshinone IIA attenuates the inflammatory response and apoptosis after traumatic injury of the spinal cord in adult rats.
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DOI：
10.1371/journal.pone.0038381
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发表时间：
2012
期刊：
影响因子：
3.7
通讯作者：
Luo ZJ
中科院分区：
文献类型：
--
作者：
Yin X;Yin Y;Cao FL;Chen YF;Peng Y;Hou WG;Sun SK;Luo ZJ
脊髓损伤包括即刻机械性损伤和继发性损伤，与创伤后的炎症反应、细胞凋亡和氧化应激有关。丹参酮IIA(Tinshinone IIA，TIA)是丹参的主要提取物之一，对多种疾病具有抗炎和抗细胞凋亡的作用。然而，TIIA治疗对脊髓损伤的影响却知之甚少。因此，本研究旨在探讨天麻对大鼠脊髓二次损伤的药理作用及其机制。脊髓损伤是通过两节段T9-T11椎板切除，在脊髓背侧使用减重装置造成的。脊髓损伤导致大鼠严重创伤，表现为运动障碍、水肿、中性粒细胞浸润、星形胶质细胞和炎性介质的产生、细胞凋亡和氧化应激。TIIA组(20 mg/kg，ip)脊髓损伤后有明显的作用：(1)改善运动功能(Basso、Beattie和Bresna han评分)；(2)减轻组织损伤程度(组织学评分)、中性粒细胞浸润(髓过氧化物酶活性)和星形胶质细胞表达；(3)抑制脊髓损伤相关通路的激活，如核因子-κB和丝裂原活化蛋白激酶信号通路；(4)减少促炎性细胞因子(肿瘤坏死因子-α、IL-1β和IL-6)和诱导型一氧化氮合酶的产生；(5)减少细胞凋亡(TUNEL染色和Bcl2和caspase-3表达)；(6)逆转氧化还原失衡。结果表明，TiIA通过抑制脊髓损伤后的炎症反应和细胞凋亡，对脊髓损伤有明显的保护作用。
Spinal cord injury (SCI), including immediate mechanical injury and secondary injury, is associated with the inflammatory response, apoptosis and oxidative stress in response to traumatic injury. Tanshinone IIA (TIIA) is one of the major extracts obtained from Salvia miltiorrhiza BUNGE, which has anti-inflammatory and anti-apoptotic effects on many diseases. However, little is known about the effects of TIIA treatment on SCI. Therefore, the aim of the present study is to evaluate the pharmacological action of TIIA on secondary damage and the underlying mechanisms of experimental SCI in rats. SCI was generated using a weight drop device on the dorsal spinal cord via a two-level T9-T11 laminectomy. SCI in rats resulted in severe trauma, characterized by locomotor disturbance, edema, neutrophil infiltration, the production of astrocytes and inflammatory mediators, apoptosis and oxidative stress. TIIA treatment (20 mg/kg, i.p.) after SCI induced significant effects: (1) improved motor function (Basso, Beattie and Bresnahan scores), (2) reduced the degree of tissue injury (histological score), neutrophil infiltration (myeloperoxidase activity) and the expression of astrocytes, (3) inhibited the activation of SCI-related pathways, such as NF-κB and MAPK signaling pathways, (4) decreased the production of pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6) and iNOS, (5) reduced apoptosis (TUNEL staining, and Bcl-2 and caspase-3 expression) and (6) reversed the redox state imbalance. The results clearly show that TIIA has a prominent protective effect against SCI through inhibiting the inflammatory response and apoptosis in the spinal cord tissue after SCI.
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