Ipriflavone as a non‐steroidal glucocorticoid receptor antagonist ameliorates diabetic cognitive impairment in mice

Nie, Rui-Fang; Lu, Jian; Xu, Rui; Yang, Juanzhen; Shen, Xiafeng; Ouyang, Xingnan; Zhu, Danyang; Huang, Yujie; Zhao, Tong; Zhao, Xin; Lu, Yin; Qian, Minyi; Wang, Jiaying; Shen, Xu

doi:10.1111/acel.13572

Cited by 12 publications

(8 citation statements)

References 46 publications

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“…Thus, synaptic functions can be protected, and learning and memory ability can be improved by inhibiting P-Tau. 47 The current study showed that the level of phosphorylated Tau inhibited by THSWD intervention, indicating that THSWD can also participate in DACD treatment by reducing the Tau phosphorylation. However, both Aβ and P-Tau production can be affected by the AGEs-RAGE pathway.…”

Section: Discussionsupporting

confidence: 51%

The Tao Hong Si Wu Decoction ameliorates diabetes‐associated cognitive dysfunction by inhibiting the formation of amyloid plaques

Cai,

Chen,

Zhang

et al. 2024

Int J Geriat Psychiatry

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ObjectivesThe herbs in Tao Hong Si Wu Decoction (THSWD) are beneficial in the treatment of cognitive impairment. However, the underlying mechanisms of THSWD in treating diabetes‐associated cognitive dysfunction (DACD) are not entirely explored. This study is aimed to investigate the therapeutic effects of THSWD in DACD model rats and the underlying mechanism.MethodsUltra‐high‐phase liquid chromatography was employed to identify the main compounds contained in the THSWD extract. DACD rat model was induced by feeding with a high‐sugar and high‐fat diet and injecting streptozotocin (35 mg/kg). DACD rats were gavaged with THSWD for 1 week. The learning and memory abilities of the rats were measured by using the Morris water maze. Western blotting was used to detect the changes in DACD rat targets. Statistical methods were used to evaluate the correlation between proteins.ResultsThe results show that THSWD effectively reduced the escape latency, hippocampal neuron damage, glycosylated hemoglobin, type A1C, and blood lipid levels in DACD rats. Furthermore, DACD rats showed significantly increased amyloid precursor protein, β‐secretase, Aβ1−40, Aβ1−42, Tau phosphorylation, and advanced glycation end products (AGEs) expression. However, THSWD treatment can reverse this phenomenon.ConclusionsTHSWD can improve the learning and memory abilities of DACD rats by inhibiting the expression of AEGs‐AGE receptors pathway, which provides an experimental basis for the clinical application of THSWD. In addition, the experiment combines pharmacological and statistical methods, which offers a new perspective for the study of Chinese herbal medicine.

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Section: Discussionsupporting

confidence: 51%

The Tao Hong Si Wu Decoction ameliorates diabetes‐associated cognitive dysfunction by inhibiting the formation of amyloid plaques

Cai,

Chen,

Zhang

et al. 2024

Int J Geriat Psychiatry

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“…Type 1 diabetes (T1DM) was induced as described previously [ 30 , 31 ]. Briefly, 7-week-old C57BL/6J mice were injected intraperitoneally with a single dose of STZ (150 mg/kg, Sigma-Aldrich) that was freshly dissolved in pH 4.5 citrate buffer.…”

Section: Methodsmentioning

confidence: 99%

ChemR23 signaling ameliorates cognitive impairments in diabetic mice via dampening oxidative stress and NLRP3 inflammasome activation

et al. 2022

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“…A raise in phosphorylation of NF-κB p65 and IκBα is detected in the hippocampus from diabetic mice after STZ administration [63,97] and higher NF-κB immunostaining is also detected in the hypothalamus, basolateral amygdala and cortex from diabetic mice [90]. Later studies have supported these observations showing that altered signaling in the hippocampus from diabetic mice includes increased protein expression of HMGB1/TLR4/NF-κB pathway, NLRP3 inflammasome [97] and the glucocorticoid receptor/ NF-κB/NLRP3/apoptosis-associated speck-like protein (ASC)/caspase-1 pathway [100].…”

Section: Streptozotocin (Stz)-induced Diabetic Micementioning

confidence: 86%

Effects of diabetes on microglial physiology: a systematic review of in vitro, preclinical and clinical studies

Vargas-Soria

García-Alloza

Corraliza-Gomez

2023

J Neuroinflammation

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Diabetes mellitus is a heterogeneous chronic metabolic disorder characterized by the presence of hyperglycemia, commonly preceded by a prediabetic state. The excess of blood glucose can damage multiple organs, including the brain. In fact, cognitive decline and dementia are increasingly being recognized as important comorbidities of diabetes. Despite the largely consistent link between diabetes and dementia, the underlying causes of neurodegeneration in diabetic patients remain to be elucidated. A common factor for almost all neurological disorders is neuroinflammation, a complex inflammatory process in the central nervous system for the most part orchestrated by microglial cells, the main representatives of the immune system in the brain. In this context, our research question aimed to understand how diabetes affects brain and/or retinal microglia physiology. We conducted a systematic search in PubMed and Web of Science to identify research items addressing the effects of diabetes on microglial phenotypic modulation, including critical neuroinflammatory mediators and their pathways. The literature search yielded 1327 records, including 18 patents. Based on the title and abstracts, 830 papers were screened from which 250 primary research papers met the eligibility criteria (original research articles with patients or with a strict diabetes model without comorbidities, that included direct data about microglia in the brain or retina), and 17 additional research papers were included through forward and backward citations, resulting in a total of 267 primary research articles included in the scoping systematic review. We reviewed all primary publications investigating the effects of diabetes and/or its main pathophysiological traits on microglia, including in vitro studies, preclinical models of diabetes and clinical studies on diabetic patients. Although a strict classification of microglia remains elusive given their capacity to adapt to the environment and their morphological, ultrastructural and molecular dynamism, diabetes modulates microglial phenotypic states, triggering specific responses that include upregulation of activity markers (such as Iba1, CD11b, CD68, MHC-II and F4/80), morphological shift to amoeboid shape, secretion of a wide variety of cytokines and chemokines, metabolic reprogramming and generalized increase of oxidative stress. Pathways commonly activated by diabetes-related conditions include NF-κB, NLRP3 inflammasome, fractalkine/CX3CR1, MAPKs, AGEs/RAGE and Akt/mTOR. Altogether, the detailed portrait of complex interactions between diabetes and microglia physiology presented here can be regarded as an important starting point for future research focused on the microglia–metabolism interface.

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Ipriflavone as a non‐steroidal glucocorticoid receptor antagonist ameliorates diabetic cognitive impairment in mice

Cited by 12 publications

References 46 publications

The Tao Hong Si Wu Decoction ameliorates diabetes‐associated cognitive dysfunction by inhibiting the formation of amyloid plaques

The Tao Hong Si Wu Decoction ameliorates diabetes‐associated cognitive dysfunction by inhibiting the formation of amyloid plaques

ChemR23 signaling ameliorates cognitive impairments in diabetic mice via dampening oxidative stress and NLRP3 inflammasome activation

Effects of diabetes on microglial physiology: a systematic review of in vitro, preclinical and clinical studies

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