Trauma is the main cause of death for people aged 1-45, and among them, traumatic brain injury (TBI) is the major condition, which causes over 50,000 deaths each year and costs over 80 billion per year. Tetrahydroxystilbene glucoside (TSG) is the active ingredient of polygonum multiflorum, a traditional Chinese herbal medicine, which presented multiple pharmacological effects, including antioxidative, anti-inflammatory, reducing blood fat and neuroprotection effects. However, the effect of TSG in promoting the recovery of the nerve system after TBI is not fully understood. PARP1 is a key enzyme in repair of the damage in DNA, which is activated by binding to DNA breaks, initiating both single-strand and double-strand DNA break repair. And we thought that overexpression of TSG might enhance the effect of TSG in TBI treatment. In this study, we firstly detected the oxidative stress response related molecules in serum samples of TBI patients and a TBI mice model, and found that oxidative stress response was activated after TBI, and TSG would reduce this effect. We further noticed that inflammation related molecules presented a similar trend with oxidative stress response related molecules. These results indicated that inflammatory response and oxidative stress processes were both activated after TBI, and reduced after TSG treatment. We further detected that the apoptosis related proteins and anti-oxidative proteins were increased after TSG treatment, and these effects were enlarged after overexpression of PARP1. We further noticed that these effects might be mediated by inhibition of the Ras/JNK signalling pathway. Thus, we thought overexpression of PARP1 might enhance the therapeutic effect of TSG in TBI treatment.

中文翻译：

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PARP1可能通过抑制Ras / JNK信号通路增强四羟基二苯乙烯葡萄糖苷在颅脑外伤中的治疗作用。

创伤是造成1-45岁人口死亡的主要原因，其中，创伤性脑损伤（TBI）是主要疾病，每年造成50,000多人死亡，每年造成的损失超过800亿美元。四羟基sti糖苷（TSG）是何首乌的有效成分，何首乌是一种中草药，具有多种药理作用，包括抗氧化，消炎，降低血脂和神经保护作用。然而，尚不完全了解TSG促进TBI后神经系统恢复的作用。PARP1是修复DNA损伤的关键酶，可通过与DNA断裂结合而激活，从而启动单链和双链DNA断裂修复。并且我们认为TSG的过表达可能会增强TSG在TBI治疗中的作用。在这个研究中，我们首先检测了TBI患者血清和TBI小鼠模型中与氧化应激反应相关的分子，发现TBI后激活了氧化应激反应，而TSG会降低这种作用。我们进一步注意到炎症相关分子与氧化应激反应相关分子呈现出相似的趋势。这些结果表明，炎症反应和氧化应激过程都在TBI后被激活，而在TSG治疗后被减轻。我们进一步检测到，TSG处理后细胞凋亡相关蛋白和抗氧化蛋白增加，而过表达PARP1后这些作用被放大。我们进一步注意到这些作用可能是通过抑制Ras / JNK信号通路来介导的。从而，