The neuroregulatory effect of cerebellar fastigial nucleus stimulation on gastric ischemia-reperfusion injury in rats.
- Author:
Xin-Wei JIANG
1
;
Dong-Shu DU
;
Jian-Fu ZHANG
;
Yong-Mei ZHANG
;
Xiao-Yan ZHOU
;
Xiao-Bo MA
Author Information
1. Laboratory of Functional Experiments, Research Center for Neurobiology, Xuzhou Medical College, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Apoptosis;
Cerebellar Nuclei;
physiology;
Electric Stimulation;
Gastric Mucosa;
cytology;
metabolism;
Hypothalamic Area, Lateral;
physiopathology;
Malondialdehyde;
metabolism;
Rats;
Rats, Sprague-Dawley;
Reperfusion Injury;
physiopathology;
Superoxide Dismutase;
metabolism
- From:
Acta Physiologica Sinica
2009;61(5):451-457
- CountryChina
- Language:Chinese
-
Abstract:
In the present study, rat model of gastric ischemia-reperfusion (GI-R) injury was established by clamping the celiac artery for 30 min followed by 1 h of reperfusion. Subsequently, the regulatory effect of electrical stimulation of cerebellar fastigial nucleus (FN) on GI-R injury and its neural mechanisms were investigated in Sprague-Dawley rats. The results are as follows. Electrical stimulation of the cerebellar FN not only obviously attenuated the GI-R injury in an intensity-dependent manner, but also decreased the apoptosis rate of gastric mucosal cells. Chemical lesion of FN eliminated the protective effect of electrical stimulation of FN on GI-R injury. Electrical stimulation of cerebellar FN decreased both the frequency and amplitude of the discharges of greater splanchnic nerve, but it could not change the discharge of greater splanchnic nerve following the lesion of the lateral hypothalamic area (LHA). After bilateral section of the greater splanchnic nerves, electrical stimulation of the FN also attenuated the GI-R injury. Chemical lesion of the LHA reversed the protective effect of electrical stimulation of FN on GI-R injury. Electrical stimulation of FN increased the activity of superoxide dismutase (SOD), but decreased the content of malondialdehyde (MDA) in gastric mucosa under GI-R. These results indicate that the cerebellar FN may regulate GI-R injury. Therefore, the cerebellar FN is an important brain site protecting the stomach against GI-R. The LHA and greater splanchnic nerves participate in the regulatory effects of cerebellar FN stimulation on GI-R injury. In addition, antioxidation may also be involved in the protection mechanism of cerebellar FN stimulation.
