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. 2015 Dec;64(5):468-472.
doi: 10.7727/wimj.2016.058. Epub 2016 Apr 29.

Protective Effects of Liquiritin on the Brain of Rats with Alzheimer's Disease

X Huang  1 , Y Wang  2 , K Ren  2
Affiliations

Protective Effects of Liquiritin on the Brain of Rats with Alzheimer's Disease

X Huang et al. West Indian Med J. 2015 Dec.

Abstract
in English, Spanish

Background: Alzheimer's disease (AD) is a sort of nerve degenerative disease with clinical manifestation of memory damage and cognitive dysfunction. Its typical pathological change is the abnormal deposition of amyloid-beta (Aβ).

Method: In this study, a rat AD model with liquiritin (LQ) interference was established to observe the effects of LQ on the AD rats' behavioural memory and primary hippocampus cells.

Results: Liquiritin had the effect of improving the rats' learning and memory ability, enhancing the activity of catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in rats' brain tissues, increasing the antioxidant ability, protecting the primary cultured hippocampal neurons and inhibiting the apoptosis induced by Aβ25-35.

Conclusion: The protective effects of LQ can be related to the enhancement of antioxidase activity and clearance of oxygen radicals.

Antecedentes:: La enfermedad de Alzheimer (EA) es una especie de enfermedad degenerativa nerviosa con manifestaciones clínicas de daño de memoria y disfunción cognitiva. Su cambio patológico típico es el depósito anormal de beta-amiloide (Aβ).

Método:: En este estudio, se estableció un modelo de ratas con EA con interferencia de liquiritin (LQ) para observar los efectos de LQ en la memoria conductual y las células primarias del hipocampo de ratas con EA.

Resultados:: El liquiritin tuvo como efectos: mejorar la capacidad de la memoria y el aprendizaje de las ratas; aumentar la actividad de catalasa (CAT), el superóxido dismutasa (SOD) y el glutatión peroxidasa (GSH-Px) en los tejidos del cerebro de ratas; aumentar la capacidad antioxidante; proteger las neuronas primarias hipocámpicas de cultivo; e inhibir la apoptosis inducida por Aβ25-35.

Conclusión:: Los efectos protectores de LQ pueden atribuirse a la mejora de la actividad antioxidasa y la depuración de los radicales de oxígeno.

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Figures

Fig. 1
Fig. 1. Cell forms of hippocampal neurons. A: Cell forms of hippocampal neurons by light microscope; B: Cell forms of hippocampal neurons marked by β-tubulin III by immunochemical observation.
Fig. 2
Fig. 2. Protective effects of liquiritin (LQ) on the primary cultured hippocampal neurons induced by Aβ25–35 (n = 3, ± s). A: optical density (OD) in MTT test; B: OD in lactate dehydrogenase (LDH) test.
* p < 0.05, ** p < 0.01 vs control group; #p < 0.05, ## p < 0.01 vs model group
Fig. 3
Fig. 3. Effects of liquiritin (LQ) on the apoptosis ratio of primary cultured hippocampal neurons induced by Aβ25-35 (n = 3, ± s). A: Control; B Model C: LQ (40 mg/kg·d) D: LQ (80 mg/kg·d); E: lQ (160 mg/kg·d); F: percentage of apoptosis.
See this image and copyright information in PMC

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