| ORIGINAL ARTICLE |
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| Year : 2019 | Volume
: 15
| Issue : 61 | Page : 335-341 |
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Astragali radix reduces ischemia-induced brain injury by inhibiting edema and expression of Aquaporin-4 in mice
Chiyeon Lim1, Byoungho Lee2, Sehyun Lim3, Se-Eun Lee4, Suin Cho4
1 Department of Medicine, College of Medicine, Dongguk University, Goyang-Si, Korea
2 Kyunghee Naseul Korean Medicine Clinic, Gyeonggi-Do, Bucheon-Si, Korea
3 Department of Nursing Science, School of Public Health, Far East University, Chungbuk, Korea
4 Department of Korean Medicine, School of Korean Medicine, Pusan National University, Yangsan, Korea
Correspondence Address:
Suin Cho
Department of Korean Medicine, School of Korean Medicine, Pusan National University, Beomeo-Ri, Mulgeum-Eup, Gyeongnam, Yangsan 50612
Korea
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/pm.pm_421_18
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Background: Astragali Radix, the dried root of Astragalus membranaceus Bunge, is a widely used herbal and traditional medicine and is viewed as a primary energizing medicinal herb that invigorates vital energy. Objective: We investigated the effects of Astragali Radix administered on ischemia-induced brain injury in a mouse model. Materials and Methods: Ischemic brain injury was induced by middle cerebral artery occlusion (MCAO) for 2 h. Methanol extracts of Astragali Radix (Amex) were then orally administered daily for 3 days. Relative cerebral blood flow was measured under ischemic conditions. Infarct volumes were measured by triphenyltetrazolium chloride staining. Changes in brain edema, brain water content, and neurological deficit (ND) scores were also measured. Aquaporin-4 (AQP-4) protein and mRNA expression were evaluated and histological changes visualized by staining with hematoxylin and eosin or cresyl violet. Results: Oral administration of Amex for 3 days after MCAO significantly reduced brain infarct volumes, edema indices, and water contents and suppressed the expression of AQP-4 at the protein and mRNA levels. However, MCAO-induced increases in ND scores were not ameliorated by Amex. Conclusion: Oral administration of Amex following onset of brain injury reduced infarct volume and brain edema. Our results suggest that reduction of AQP-4 protein and mRNA expression is a possible mechanism for these effects.
Abbreviations used: r-tPA: Recombinant tissue plasminogen activator; BBB: Blood–brain barrier; Nrf2: Nuclear factor erythroid 2-related factor 2; Foxp3: Forkhead box P3; VEGF: Vascular endothelial growth factor; MMP-9: Matrix metallopeptidase-9; TRPC6: Transient receptor potential cation channel subfamily C member 6; p-CREB: Phospho-cyclic AMP response element binding; JNK3: C-Jun N-terminal kinase 3; SPF: Specific-pathogen-free; DMSO: Dimethyl sulfoxide; TTC: 2,3,5-triphenyltetrazolium chloride; PBS: Phosphate-buffered saline; PFA: Paraformaldehyde; OCT: Optimum cutting temperature; AQP-4: Aquaporin-4; SDS-PAGE: Sodium dodecyl sulfate-polyacrylamide gels by electrophoresis; PVDF: Polyvinylidene difluoride; RT-PCR: Reverse transcription polymerase chain reaction.
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