The kallikrein-kinin system (KKS) is an important endogenous pathway involved in a serial of physiological and pathological changes, such as blood pressure controlling and inflammation. It has been proved to exert a role in several disorders of central nerve system, including epilepsy. Studies of different animal models, including pilocarpine-indued, audiogenic kindling and amygdaloid kindling animal models, have showed that the expressions of the bradykinin receptors B1 and B2 were both up-regulated, or showed that the relative ratio of bradykinin receptor B1 to B2 was elevated. In patients with temporal lobe epilepsy and hippocampal sclerosis, the levels of bradykinin receptors B1 and B2 in pyramidal neurons and kallikrein 1 in astrocytes were all over-expressed in hippocampus. It has been suggested that bradykinin receptor B1 may be pro-convulsant while bradykinin receptor B2 may be linked to neuroprotection. The possible underlying mechanisms include promoting blood-brain-barrier disruption, inducing the release of excitatory amino acids, and mediating the inflammatory response. KKS may become a novel target for prevention and treatment of epilepsy. This paper summarizes the advances in research on KKS and epileptogenesis.
ZOU Jing, LU Qinchi.
Kallikrein-kinin system and epileptogenesis[J]. Journal of Neurology and Neurorehabilitation. 2016, 12(3): 152-156 https://doi.org/10.12022/jnnr.2016-0048
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