Neuroprotective effect of batroxobin on experimental intracerebral hemorrhage in rats.
- Author:
Li QI
1
;
Zhi DONG
;
Jie MA
Author Information
1. Department of Pharmacology, Pharmacy College, Chongqing Medical University, Key Laboratory of Biochemistry and Molecular Pharmacology, Chongqing 400016, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Batroxobin;
pharmacology;
therapeutic use;
Behavior, Animal;
drug effects;
Brain;
pathology;
Brain Edema;
drug therapy;
etiology;
Calcium;
metabolism;
Cerebral Hemorrhage;
chemically induced;
complications;
metabolism;
physiopathology;
Collagenases;
Female;
Male;
Malondialdehyde;
metabolism;
Neurons;
metabolism;
Neuroprotective Agents;
pharmacology;
therapeutic use;
Random Allocation;
Rats;
Rats, Sprague-Dawley;
Superoxide Dismutase;
metabolism
- From:
Acta Pharmaceutica Sinica
2009;44(4):338-343
- CountryChina
- Language:Chinese
-
Abstract:
This study is to investigate if batroxobin has the protective effect against nerve injury caused by cerebral hemorrhage in rats and its possible mechanism. Animals were divided into sham group, model group, batroxobin 4, 8, and 16 BU x kg(-1) groups and nimodipine positive control group. On the brain stereotaxic apparatus, the rat intracerebral hemorrhage model was established by injecting collagenase with microinjector into the brain caudate nucleus which was located according to the brain stereotaxic atlas. Neuroethology of the rats was estimated. The brain tissue pathomorphology was observed with electron microscope. The water content of the brain tissue was quantitated with wet/dry weight measurement. SOD and MDA were determined according to the kit procedure, and free Ca2+ concentration in neurocyte was measured by fluorospectrophotometer. As shown in results, batroxobin could improve neuroethology scale of the rats, relieve histiocyte edema and bleeding degree. The water content of the brain tissue, MDA and free Ca2+ concentration were reduced and SOD activity was raised in batroxobin treatment groups. Therefore, it is possible that batroxobin has some protective effect against nerve injury caused by cerebral hemorrhage in rats, and its mechanism maybe relate to lessening brain edema, reducing MDA content, raising SOD activity, and inhibiting calcium overload.
