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Upregulation of Nrf2 signaling: A key molecular mechanism of Baicalin's neuroprotective action against diabetes-induced cognitive impairment.
Zheng, Yanfang; Wang, Chenxiang; Liu, Wenjing; Chen, Jiaying; Sun, Yibin; Chang, Dennis; Wang, Huan; Xu, Wen; Lu, Jin-Jian; Zhou, Xian; Huang, Mingqing.
Afiliación
  • Zheng Y; College of Pharmacy, Fujian Key Laboratory of Chinese Materia Medica, Fujian University of Traditional Chinese Medicine, Fuzhou 350108, China.
  • Wang C; College of Pharmacy, Fujian Key Laboratory of Chinese Materia Medica, Fujian University of Traditional Chinese Medicine, Fuzhou 350108, China.
  • Liu W; College of Pharmacy, Fujian Key Laboratory of Chinese Materia Medica, Fujian University of Traditional Chinese Medicine, Fuzhou 350108, China.
  • Chen J; College of Pharmacy, Fujian Key Laboratory of Chinese Materia Medica, Fujian University of Traditional Chinese Medicine, Fuzhou 350108, China.
  • Sun Y; College of Pharmacy, Fujian Key Laboratory of Chinese Materia Medica, Fujian University of Traditional Chinese Medicine, Fuzhou 350108, China.
  • Chang D; NICM Health Research Institute, Western Sydney University, Westmead, NSW 2145, Australia.
  • Wang H; College of Pharmacy, Fujian Key Laboratory of Chinese Materia Medica, Fujian University of Traditional Chinese Medicine, Fuzhou 350108, China.
  • Xu W; College of Pharmacy, Fujian Key Laboratory of Chinese Materia Medica, Fujian University of Traditional Chinese Medicine, Fuzhou 350108, China.
  • Lu JJ; State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Avenida da Universidade, Taipa, Macao 999078, China. Electronic address: jinjianlu@um.edu.mo.
  • Zhou X; NICM Health Research Institute, Western Sydney University, Westmead, NSW 2145, Australia. Electronic address: p.zhou@westernsydney.edu.au.
  • Huang M; College of Pharmacy, Fujian Key Laboratory of Chinese Materia Medica, Fujian University of Traditional Chinese Medicine, Fuzhou 350108, China. Electronic address: hmq1115@126.com.
Biomed Pharmacother ; 174: 116579, 2024 May.
Article en En | MEDLINE | ID: mdl-38631145
ABSTRACT
BACKGROUND AND

AIM:

Diabetes-associated cognitive impairment (DCI) is a prevalent complication of diabetes. However, there is a lack of viable strategies for preventing and treating DCI. This study aims to explore the efficacy of baicalin (Bai) in attenuating DCI and elucidating the underlying mechanisms. EXPERIMENTAL PROCEDURE GK rats fed a high-fat and high-glucose diet were utilized to investigate the therapeutic potential of Bai. Cognitive function was assessed using the Morris water maze and novel object recognition tests. To gain insight into the molecular mechanisms underlying Bai's neuro-protective effects, co-cultured BV2/HT22 cells were established under high-glucose (HG) stimulation. The modes of action of Bai were subsequently confirmed in vivo using the DCI model in db/db mice. KEY

RESULTS:

Bai restored cognitive and spatial memory and attenuated neuron loss, along with reducing expressions of Aß and phosphorylated Tau protein in diabetic GK rats. At the cellular level, Bai exhibited potent antioxidant and anti-inflammatory effects against HG stimulation. These effects were associated with the upregulation of Nrf2 and supressed Keap1 levels. Consistent with these in vitro findings, similar mechanisms were observed in db/db mice. The significant neuroprotective effects of Bai were abolished when co-administered with ATRA, a Nrf2 blocker, in db/db mice, confirming that KEAP1-Nrf2 signaling pathway was responsible for the observed effect. CONCLUSIONS AND IMPLICATIONS Bai demonstrates a great therapeutic potential for attenuating DCI. The antioxidant defense and anti-inflammatory actions of Bai were mediated through the KEAP1-Nrf2 axis. These findings advance our understanding of potential treatment approaches for DCI, a common complication associated with diabetes.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Flavonoides / Transducción de Señal / Regulación hacia Arriba / Fármacos Neuroprotectores / Factor 2 Relacionado con NF-E2 / Disfunción Cognitiva Límite: Animals Idioma: En Revista: Biomed Pharmacother Año: 2024 Tipo del documento: Article Pais de publicación: Francia
Texto completo
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XML
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Flavonoides / Transducción de Señal / Regulación hacia Arriba / Fármacos Neuroprotectores / Factor 2 Relacionado con NF-E2 / Disfunción Cognitiva Límite: Animals Idioma: En Revista: Biomed Pharmacother Año: 2024 Tipo del documento: Article Pais de publicación: Francia