HSYA alleviates secondary neuronal death through attenuating oxidative stress, inflammatory response, and neural apoptosis in SD rat spinal cord compression injury.
HSYA alleviates secondary neuronal death through attenuating oxidative stress, inflammatory response, and neural apoptosis in SD rat spinal cord compression injury.
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HSYA 通过减轻 SD 大鼠脊髓压迫损伤中的氧化应激、炎症反应和神经细胞凋亡来减轻继发性神经元死亡
DOI：
10.1186/s12974-017-0870-1
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发表时间：
2017-05-03
影响因子：
9.3
通讯作者：
Wang KZ
中科院分区：
文献类型：
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作者：
Pei JP;Fan LH;Nan K;Li J;Dang XQ;Wang KZ
羟基红花黄色素A（HSYA）是从红花中提取的黄色素的主要活性成分，该化合物在体外和体内均具有强大的神经保护作用。然而，HSYA的潜在机制尚未完全阐明。本研究旨在探讨HSYA对大鼠脊髓压迫性损伤的保护作用及其机制。将Sprague-Dawley大鼠分为假手术组、对照组和HSYA组（每组n = 30）。在T9 ~ T10节段硬脊膜上应用血管夹（50 g，1 min）造成脊髓损伤（SCI）模型。损伤的动物通过腹膜内注射给予HSYA（在损伤后1和6小时给予8 mg/kg，然后14 mg/kg，以24小时的时间间隔共7天）或等体积的盐水。从本实验中，我们发现大鼠SCI导致严重的创伤，其特征在于组织损伤、脂质过氧化、中性粒细胞浸润、炎症介质释放和神经元凋亡。然而，HSYA治疗显著降低了以下方面：（1）组织损伤程度（2）中性粒细胞浸润（髓过氧化物酶活性）;（3）氧化应激（超氧化物歧化酶、丙二醛和一氧化氮）;（4）促炎细胞因子表达（5）核因子-κB活化;（6）凋亡（末端脱氧核苷酸转移酶dUTP缺口末端标记染色和半胱氨酸-天冬氨酸蛋白酶-3活性）。此外，在一组单独的实验中，我们清楚地表明，HSYA治疗显着改善肢体功能的恢复（如Basso，Beattie和Bresnahan行为恢复评分所评估的）。用HSYA治疗抑制与大鼠SCI相关的氧化应激、炎症反应和凋亡事件的发展，表明HSYA是用于人类SCI治疗的潜在神经保护剂。
Hydroxysafflor yellow A (HSYA) is a major active component of yellow pigment extracted from safflowers; this compound possesses potent neuroprotective effects both in vitro and in vivo. However, underlying mechanism of HSYA is not fully elucidated. The present study investigated the protective effects of HSYA in rat spinal cord compression injury model and related mechanisms involved. Sprague–Dawley rats were divided as Sham, Control, and HSYA groups (n = 30 per group). Spinal cord injury (SCI) model was induced by application of vascular clips (force of 50 g, 1 min) to the dura at T9–T10 level of vertebra. Injured animals were administered with either HSYA (8 mg/kg at 1 and 6 h after injury, then 14 mg/kg, for a total of 7 days at 24-h time intervals) or equal volume of saline by intraperitoneal injection. From this experiment, we discovered that SCI in rats resulted in severe trauma, which is characterized by tissue damage, lipid peroxidation, neutrophil infiltration, inflammation mediator release, and neuronal apoptosis. However, HSYA treatment significantly reduced the following: (1) degree of tissue injury (histological score) and edema; (2) neutrophil infiltration (myeloperoxidase activity); (3) oxidative stress (superoxide dismutase, malondialdehyde, and nitric oxide); (4) pro-inflammatory cytokine expression (tumor necrosis factor-α, interleukin-6, inducible nitric oxide synthase, cyclooxygenase-2); (5) nuclear factor-κB activation; (6) apoptosis (terminal deoxynucleotidyl transferase dUTP nick end labeling staining and cysteine-aspartic protease-3 activity). Moreover, in a separate set of experiments, we clearly demonstrated that HSYA treatment significantly ameliorated recovery of limb function (as evaluated by Basso, Beattie, and Bresnahan behavioral recovery scores). Treatment with HSYA restrains development of oxidative stress, inflammation response, and apoptotic events associated with SCI of rats, demonstrating that HSYA is a potential neuroprotectant for human SCI therapy.