Glucosides of chaenomeles speciosa attenuate ischemia/reperfusion-induced brain injury by regulating NF-κB P65/TNF-α in mouse model.
- Author:
Jing MA
1
;
Wenlong HE
2
;
Chongyang GAO
1
;
Ruiyun YU
1
;
Peng XUE
2
;
Yongchao NIU
3
Author Information
1. Department of Neurology, Xinxiang Central Hospital, Xinxiang 453000, Henan Province, China.
2. Department of General Medicine, Xinxiang Central Hospital, Xinxiang 453000, Henan Province, China.
3. Department of Magnetic Resonance, Xinxiang Central Hospital, Xinxiang 453000, Henan Province, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Brain;
drug effects;
Brain Injuries;
drug therapy;
Gene Expression Regulation;
drug effects;
Glucosides;
pharmacology;
therapeutic use;
Mice;
Mice, Inbred C57BL;
NF-kappa B;
genetics;
Oxidative Stress;
drug effects;
Plant Extracts;
pharmacology;
Random Allocation;
Rosaceae;
chemistry;
Tumor Necrosis Factor-alpha;
genetics
- From:
Journal of Zhejiang University. Medical sciences
2019;48(3):289-295
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To investigate the effect and mechanism of glucosides of chaenomeles speciosa (GCS) on ischemia/reperfusion-induced brain injury in mouse model.
METHODS:Fifty 8-week C57BL/C mice were randomly divided into five groups with 10 in each group:sham group, model group, GCS 30 mg/kg group, GCS 60 mg/kg group and GCS 90 mg/kg group, and the GCS was administrated by gavage (once a day) for 14 d. HE staining was performed to investigate the cell morphology; the Zea-Longa scores were measured for neurological activity; TUNEL staining was performed to investigate the cell apoptosis; ELISA was used to detected the oxidative stress and inflammation; Western Blot was performed to investigate the key pathway and neurological functional molecules.
RESULTS:Compared with the sham group, the brain tissues in model group were seriously damaged, presenting severe cell apoptosis, oxidative stress and inflammation, associated with increased NF-κB P65 and TNF-α levels as well as decreased myelin associate glycoprotein (MAG) and oligodendrocyte-myelin glycoprotein (OMgp)levels (all <0.01). Compared with the model group, the brain tissues in GCS groups were ameliorated, and cell apoptosis, oxidative stress and inflammation were inhibited, associated with decreased NF-κB P65 and TNF-α levels as well as increased MAG and OMgp levels (all <0.01), which were more markedly in GCS 60 mg/kg group.
CONCLUSIONS:GCS can inhibit the NF-κB P65 and TNF-α, reduce the oxidative stress and inflammation, decrease the cell apoptosis in mouse ischemia/reperfusion-induced brain injury model, and 60 mg/kg GCS may be the optimal dose.
