Department of Neurology, Jinling Hospital, Nanjing University School of Medicine, Nanjing 210002, China.
Biochem Biophys Res Commun. 2011 Apr 8;407(2):283-7. doi: 10.1016/j.bbrc.2011.02.112. Epub 2011 Mar 3.
Systemic or local delivery of human tissue kallikrein gene (hTK) has been shown to be an effective strategy to alleviate cerebral ischemia/reperfusion (I/R) injury, and tissue kallikrein (TK) administration can suppress glutamate- or acidosis-mediated neurotoxicity in vitro. In the present study, the role of TK in hypoxia/reoxygenation (H/R) induced neuronal cell death was investigated. We found that TK administration could remarkably alleviate H/R-induced neuronal injury by reduction of LDH release and promotion of neuron viability. The protective effects of TK could be counteracted by bradykinin B2 receptor (B2R) antagonist HOE140, which could suppress up-regulation of TK on the ERK signal pathway under H/R condition. These results indicate that TK plays an important role in preventing neurons from H/R damage at least partially through the TK-B2R-ERK1/2 pathway.
系统或局部递送人组织激肽释放酶基因（hTK）已被证明是减轻脑缺血/再灌注（I / R）损伤的有效策略，并且组织激肽（TK）的给药可以体外抑制谷氨酸或酸中毒介导的神经毒性。在本研究中，研究了 TK 在缺氧/复氧（H / R）诱导的神经元细胞死亡中的作用。我们发现，TK 的给药可通过减少 LDH 释放和促进神经元活力来显著减轻 H / R 诱导的神经元损伤。TK 的保护作用可被缓激肽 B2 受体（B2R）拮抗剂 HOE140 拮抗，HOE140 可抑制 H / R 条件下 TK 对 ERK 信号通路的上调。这些结果表明，TK 通过 TK-B2R-ERK1 / 2 通路至少部分地在防止神经元免受 H / R 损伤中起重要作用。
