Intracerebroventricular injection of Aβ1-42 combined with two-vessel occlusion accelerate Alzheimer’s disease development in rats

Dai, Shi Jie; Zhang, Jie Ying; Yu, Bin; Zhang, Xiao; Lin, Lu; Fu, Yun; Zhang, Yu Jia; Li, Chang Yu; Yang, Yuan

doi:10.1016/j.prp.2018.07.020

Cited by 11 publications

(4 citation statements)

References 53 publications

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“…The sections were then incubated with the primary rabbit anti-matrix metalloprotease-13 antibody (Absin Bioscience, Shanghai, China), and secondary antibody binding was visualized using 3,3-diaminobenzoic acid. For quantitative immunohistochemical assessment, five nonoverlapping fields per section were randomly captured by stereomicroscopy (SMZ745T, Nikon, Tokyo, Japan animals/experimental group were considered for comparison and statistical analyses [29].…”

Section: Immunocytochemistrymentioning

confidence: 99%

Gut microbiome dysbiosis alleviates the progression of osteoarthritis in mice

et al. 2020

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Gut microbiota dysbiosis has been studied under the pathological conditions of osteoarthritis (OA). However, the effect of antibiotic-induced gut flora dysbiosis on OA remains incompletely understood at present. Herein, we used a mouse (8 weeks) OA model of destabilization of the medial meniscus (DMM) and gut microbiome dysbiosis induced by antibiotic treatment with ampicillin and neomycin for 8 weeks. The results show that antibiotic-induced intestinal microbiota dysbiosis reduced the serum level of lipopolysaccharide (LPS) and the inflammatory response, such as suppression of the levels of tumour necrosis factor-α (TNF-α) and interleukin-6 (IL-6), which can lead to decreased matrix metalloprotease-13 (MMP-13) expression and improvement of OA after joint injury. In addition, trabecular thickness (Tb.Th) and osteophyte scores were increased significantly in antibiotic-induced male mice compared with female mice. We further used network correlation analysis to verify the effect of gut microbiota dysbiosis on OA. Therefore, this study contributes to our understanding of the gut-joint axis in OA and reveals the relationship between the inflammatory response, sex and gut microbiota, which may provide new strategies to prevent the symptoms and long-term sequelae of OA.

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Section: Immunocytochemistrymentioning

confidence: 99%

Gut microbiome dysbiosis alleviates the progression of osteoarthritis in mice

et al. 2020

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“…Akt downregulation and NF-κB upregulation have been observed in microglial cells after Aβ42 incubation. Moreover, LY294002, an Akt inhibitor, has been reported to enhance the expression of M1 marker [29]. The above evidence suggests a close relationship between MA and PI3K/AKT signaling.…”

Section: Discussionmentioning

confidence: 81%

C16 Peptide and Ang-1 Improve Functional Disability and Pathological Changes in an Alzheimer’s Disease Model Associated with Vascular Dysfunction

Wang

Cai

et al. 2022

Pharmaceuticals

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Alzheimer’s disease (AD) is a neurological disorder characterized by neuronal cell death, tau pathology, and excessive inflammatory responses. Several vascular risk factors contribute to damage of the blood–brain barrier (BBB), secondary leak-out of blood vessels, and infiltration of inflammatory cells, which aggravate the functional disability and pathological changes in AD. Growth factor angiopoietin-1 (Ang-1) can stabilize the endothelium and reduce endothelial permeability by binding to receptor tyrosine kinase 2 (Tie2). C16 peptide (KAFDITYVRLKF) selectively binds to integrin ανβ3 and competitively inhibits leukocyte transmigration into the central nervous system by interfering with leukocyte ligands. In the present study, 45 male Sprague-Dawley (SD) rats were randomly divided into three groups: vehicle group, C16 peptide + Ang1 (C + A) group, and sham control group. The vehicle and C + A groups were subjected to two-vessel occlusion (2-VO) with artery ligation followed by Aβ1-42 injection into the hippocampus. The sham control group underwent sham surgery and injection with an equal amount of phosphate-buffered saline (PBS) instead of Aβ1-42. The C + A group was administered 1 mL of drug containing 2 mg of C16 and 400 µg of Ang-1 daily for 2 weeks. The sham control and vehicle groups were administered 1 mL of PBS for 2 weeks. Our results showed that treatment with Ang-1 plus C16 improved functional disability and reduced neuronal death by inhibiting inflammatory cell infiltration, protecting vascular endothelial cells, and maintaining BBB permeability. The results suggest that these compounds may be potential therapeutic agents for AD and warrant further investigation.

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“…The 2-VO operation results in the insufficiency of the persistent cerebral blood flow, which was partly similar to the clinical characteristics of VD patients ( 34 , 35 ), so we then used laser doppler flowmetry to explore the effects on cerebral blood flow. As shown in Fig.…”

Section: Resultsmentioning

confidence: 93%

Gardenia jasminoides J. Ellis extract GJ-4 attenuates hyperlipidemic vascular dementia in rats via regulating PPAR-γ-mediated microglial polarization

Liu

Zang

Shang

et al. 2022

Food & Nutrition Research

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Background: GJ-4 is extracted from Gardenia jasminoides J. Ellis (Fructus Gardenia) with crocin composition and has been demonstrated to improve memory deficits in several dementia models in our previous studies.Objective: This study aimed to evaluate the effects of GJ-4 on hyperlipidemic vascular dementia (VD) and explore the underlying mechanisms. Design: In the current study, we employed a chronic hyperlipidemic VD rat model by permanent bilateral common carotid arteries occlusion (2-VO) based on high-fat diet (HFD), which is an ideal model to mimic the clinical pathogenesis of human VD. Results: Our results showed that GJ-4 could significantly reduce serum lipids level and improve cerebral blood flow in hyperlipidemic VD rats. Additionally, treatment with GJ-4 remarkedly ameliorated memory impairment and alleviated neuronal injury. Mechanistic investigation revealed that the neuroprotective effects of GJ-4 might be attributed to the inhibition of microglia-mediated neuro-inflammation via regulating the M1/M2 polarization. Our data further illustrated that GJ-4 could regulate the phenotype of microglia through activating the peroxisome proliferator-activated receptor-γ (PPAR-γ) and subsequently inhibited nuclear factor-κB (NF-κB) nuclear translocation and increased CCAAT/enhancer-binding protein β (C/EBPβ) expression. Conclusion:Our results implied that GJ-4 might be a promising drug to improve VD through the regulation of microglial M1/M2 polarization and the subsequent inhibition of neuro-inflammation.Popular scientific summary 1. Gardenia jasminoides J. Ellis extract GJ-4 remarkedly improved dyslipidemia and memory disorders in hyperlipidemic vascular dementia (VD) rats. 2. The study showed that GJ-4 significantly inhibited microglial activation and modified microglial M1/M2 polarization by regulating PPAR-γ signaling pathway. 3. GJ-4 might be a promising drug to improve VD through the regulation of microglial M1/M2 polarization and the subsequent inhibition of neuro-inflammation.

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Intracerebroventricular injection of Aβ1-42 combined with two-vessel occlusion accelerate Alzheimer’s disease development in rats

Cited by 11 publications

References 53 publications

Gut microbiome dysbiosis alleviates the progression of osteoarthritis in mice

Gut microbiome dysbiosis alleviates the progression of osteoarthritis in mice

C16 Peptide and Ang-1 Improve Functional Disability and Pathological Changes in an Alzheimer’s Disease Model Associated with Vascular Dysfunction

Gardenia jasminoides J. Ellis extract GJ-4 attenuates hyperlipidemic vascular dementia in rats via regulating PPAR-γ-mediated microglial polarization

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