Reduction of angiotensin II in the cerebrospinal fluid of patients with multiple sclerosis
Reduction of angiotensin II in the cerebrospinal fluid of patients with multiple sclerosis
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DOI：
10.1177/1352458507085760
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发表时间：
2008-05-01
影响因子：
5.8
通讯作者：
Kira, J. I.
中科院分区：
文献类型：
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作者：
Kowajiri, M.;Mogi, M.;Kira, J. I.
我们先前通过血管紧张素II 2型受体信号转导证明了血管紧张素II在神经损伤后作为一个重要的神经保护因子发挥作用。虽然已知该通路在实验性自身免疫性脑脊髓炎的发生发展中起重要作用，但多发性硬化(MS)患者脑脊液(CSF)中血管紧张素II的水平从未被研究过。为了阐明血管紧张素II在MS中的意义，我们用建立的酶联免疫吸附分析法检测了MS患者(n=21)、炎性神经病(IN)患者(n=23)和对照组(n=24)脑脊液中血管紧张素II的浓度。脑脊液中血管紧张素II水平MS组为3.79+/-1.54pg/ml，IN组为5.13+/-2.27pg/ml，对照组为6.71+/-2.65pg/ml。MS组脑脊液中血管紧张素II水平明显低于对照组(P=0.00057)。脑脊液中血管紧张素II浓度与库尔茨克扩展残疾状态量表评分呈负相关(p=0.0847)。这些发现提示鞘内血管紧张素II水平降低可能与MS的神经损伤和修复过程异常有关。
We previously demonstrated that angiotensin II acts as a crucial neuroprotective factor after neural injury through angiotensin II type-2 (AT2) receptor signaling. Although the pathway is known to play an important role in the development of experimental autoimmune encephalomyelitis, cerebrospinal fluid (CSF) angiotensin II levels in patients with multiple sclerosis (MS) have never been studied. To clarify the significance of angiotensin II in MS, we assayed angiotensin II concentrations using an established enzyme-linked immunoabsorbent assay in CSF samples from patients with MS (n=21), patients with inflammatory neuropathies (IN) (n=23) and control individuals who did not have either of the neurological diseases or any other disease that might affect the angiotensin II levels in the CSF (control) (n=24). Angiotensin II levels in the CSF were 3.79 +/- 1.54 pg/ml in the MS group, 5.13 +/- 2.27 pg/ml in the IN group and 6.71 +/- 2.65 pg/ml in the control group. The angiotensin II levels in the CSF of the MS group were significantly lower than in the control group (p = 0.00057). Angiotensin II concentration in the CSF tended to have a negative correlation with the Kurtzke's Expanded Disability Status Scale scores during MS relapse (p = 0.0847). These findings suggest that reduced levels of intrathecal angiotensin II may be related to the abnormal neural damage and repair processes in MS.