Title |
Buyang huanwu decoction promotes angiogenesis via vascular endothelial growth factor receptor-2 activation through the PI3K/Akt pathway in a mouse model of intracerebral hemorrhage
|
---|---|
Published in |
BMC Complementary Medicine and Therapies, March 2015
|
DOI | 10.1186/s12906-015-0605-8 |
Pubmed ID | |
Authors |
Han-Jin Cui, A-Li Yang, Hua-Jun Zhou, Cong Wang, Jie-Kun Luo, Yuan Lin, Yan-Xia Zong, Tao Tang |
Abstract |
Intracerebral hemorrhage (ICH) is a fatal subtype of stroke that lacks effective treatments. Angiogenesis following ICH is an important response mediating brain recovery and repair. Phosphorylation of vascular endothelial growth factor receptor 2 (pVEGFR2) via PI3K/Akt signaling plays a key role in mediating cellular processes involved in repair, such as mitogenesis, angiogenesis, and vascular permeability. This study aimed to investigate the potential effects of Buyang Huanwu Decoction (BYHWD), a traditional Chinese medicine formula, on angiogenesis by VEGFR2 activation through the phosphatidylinositol 3 kinase (PI3K)/Akt signaling pathway in a mouse model of ICH. Adult male Kunming mice (n = 50) were randomly assigned into sham and ICH-operated groups and treated with one of the followings SU5416 (VEGFR2 inhibitor), BYHWT and BYHWT + SU5416. ICH was induced in mice by injecting collagenase (type VII) into the right globus pallidus of the mouse brain. BYHWD (4.36 g/kg) was administrated in mice by intragastric infusion. Neurological function was evaluated in mice by a modified Neurological Severity Scores (mNSS) as well as corner turn and foot-fault tests. Angiogenesis was examined by intraperitoneal injection of 5-bromodeoxyuridine (BrdU) in mice to quantify new brain vessel growth. SU5416 treatment and assessment of VEGFR2 phosphorylation as well as alterations in PI3K/Akt signaling were performed to determine whether the effect of BYHWD on angiogenesis was partly mediated by phosphorylation of VEGFR2 via the PI3K/Akt signaling pathway. We show that BYHWD treated mice exhibited (i) significantly better recovery from neurological dysfunction, (ii) increased BrdU(+) nuclei in vWF(+) dilated brain vessels and (iii) higher VEGFR2 phosphorylation immunoreactivity in brain microvessels (P <0.05), (iv) higher expression of PI3K and pAkt at the protein level (P <0.05) when compared to untreated ICH mice. These beneficial effects were reversed by SU5416 (P <0.05). BYHWD promoted neurological recovery and angiogenesis after ICH in mice by enhancing VEGFR2 phosphorylation through the PI3K/Akt signaling pathway. |
Mendeley readers
Geographical breakdown
Country | Count | As % |
---|---|---|
Unknown | 15 | 100% |
Demographic breakdown
Readers by professional status | Count | As % |
---|---|---|
Student > Ph. D. Student | 3 | 20% |
Lecturer | 2 | 13% |
Student > Doctoral Student | 2 | 13% |
Lecturer > Senior Lecturer | 1 | 7% |
Student > Master | 1 | 7% |
Other | 1 | 7% |
Unknown | 5 | 33% |
Readers by discipline | Count | As % |
---|---|---|
Neuroscience | 2 | 13% |
Medicine and Dentistry | 2 | 13% |
Pharmacology, Toxicology and Pharmaceutical Science | 1 | 7% |
Biochemistry, Genetics and Molecular Biology | 1 | 7% |
Agricultural and Biological Sciences | 1 | 7% |
Other | 2 | 13% |
Unknown | 6 | 40% |