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首页> 外文期刊>Life sciences >Calcium-independent CaMKII activity is involved in ginsenoside Rb1-mediated neuronal recovery after hypoxic damage.
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Calcium-independent CaMKII activity is involved in ginsenoside Rb1-mediated neuronal recovery after hypoxic damage.

机译：缺氧损伤后人参皂甙Rb1介导的神经元恢复中涉及非钙依赖性CaMKII活性。

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摘要

Recent studies have indicated that Ginsenoside Rb1, one of the major components of ginseng root, may play an important role in protecting cells from damage. Here, we investigated the neuroprotective activity of Rb1 after hypoxic injury in young rats. About 50% animals were dead by exposing hypoxic condition three times in three consecutive days. Then, the pretreatment with Rb1 prior to hypoxic stimulation reduced animal death to 12%, and also significantly reduced the recovery time from hypoxia-related, compromised symptoms in survived animals. Rb1 also significantly reduced levels of lactate dehydrogenase (LDH) release from primary hippocampal neurons which were maintained at low oxygen concentration, indicating increased neuronal survival by Rb1. Ca(2+)/calmodulin-dependent kinase II (CaMKII) activity in the hippocampal tissues of hypoxia-induced rats was decreased to about 50% of the control animal. Then Rb1-treatment prior to hypoxic stimulation significantly elevated Ca(2+)-independent kinase II activity when measured 48 hr after hypoxic stimulation. Thus, the present data suggest that calcium independent CaMKII activity may be involved in the process of ginsenoside Rb1-mediated recovery of neuronal cells after hypoxic damage.
机译：最近的研究表明，人参根的主要成分之一人参皂甙Rb1可能在保护细胞免受损伤中起重要作用。在这里，我们调查了幼鼠低氧损伤后Rb1的神经保护活性。连续三天三次暴露于低氧条件下，约有50％的动物死亡。然后，在缺氧刺激之前用Rb1进行的预处理将动物死亡降低到12％，并且还大大减少了存活动物中与缺氧相关的受损症状的恢复时间。 Rb1还显着降低了维持在低氧浓度下的原代海马神经元释放的乳酸脱氢酶（LDH）的水平，表明Rb1增加了神经元存活。缺氧诱导的大鼠海马组织中的Ca（2 +）/钙调蛋白依赖性激酶II（CaMKII）活性降低至对照动物的约50％。然后低氧刺激后48小时测量时，低氧刺激之前的Rb1处理显着提高了Ca（2 +）-独立的激酶II活性。因此，目前的数据表明缺氧损伤后，钙独立的CaMKII活性可能参与人参皂苷Rb1介导的神经元细胞恢复过程。

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