The present study was undertaken to explore the role of total flavones of Camellia (TFC) on cerebral injury following subarachnoid hemorrhage (SAH) in rats. We showed that the increase of malondialdehyde (MDA) level in brain tissues, leakages of neuron-specifc enolase (NSE) and lactate dehydrogenase (LDH) from brain tissues to serum at 48 h after SAH were significantly blocked by TFC treatment. Besides, TFC treatment could reduce brain edema and the Bax/Bcl-2 ratio in hippocampal tissues at mRNA and protein levels at 48 h after SAH. In addition, and the reduction of neurological scores at 7d after SAH were significantly inhibited by TFC treatment. We next sought to demonstrate the role of TFC on cognitive rehabilitation and the tau phosphorylation in hippocampal tissues at 30d after SAH. Not surprisingly, cognitive dysfunction and the upregulation of tau phosphorylation at Ser262 (p-tau-Ser262) in hippocampal tissues were markedly reduced by TFC treatment. These findings suggested that TFC has protective effect on SAH-induced EBI and subsequent cognitive dysfunction, which may be related to downregulating the Bax/Bcl-2-related apoptosis pathway and inhibition of tau phosphorylation.

中文翻译：

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山茶总黄酮对大鼠蛛网膜下腔出血早期脑损伤和认知功能障碍的神经保护作用。

本研究旨在探讨山茶总黄酮 (TFC) 对大鼠蛛网膜下腔出血 (SAH) 后脑损伤的作用。我们发现 TFC 处理显着阻断了 SAH 后 48 小时脑组织中丙二醛 (MDA) 水平的增加、神经元特异性烯醇化酶 (NSE) 和乳酸脱氢酶 (LDH) 从脑组织向血清的泄漏。此外，TFC 治疗可以减少 SAH 后 48 小时 mRNA 和蛋白质水平的海马组织中的脑水肿和 Bax/Bcl-2 比值。此外，TFC 治疗显着抑制了 SAH 后第 7 天神经系统评分的降低。我们接下来试图证明 TFC 在 SAH 后 30 天对认知康复和海马组织中 tau 磷酸化的作用。这并不奇怪，TFC 治疗显着降低了认知功能障碍和海马组织中 Ser262 (p-tau-Ser262) tau 磷酸化的上调。这些发现表明TFC对SAH诱导的EBI和随后的认知功能障碍具有保护作用，这可能与下调Bax/Bcl-2相关的凋亡通路和抑制tau磷酸化有关。