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4 results on '"Jinyu Mei"'

1. Soluble β-amyloid impaired the GABA inhibition by mediating KCC2 in early APP/PS1 mice

Author

Jinyu Mei, Yuenan Chen, Zhihan Wu, Yujie Cheng, Yong Li, Jiyao Ma, Ming Chen, and Yuan Zhou

Subjects
medicine.medical_specialty, Health (social science), Hippocampus, Mice, Transgenic, General Biochemistry, Genetics and Molecular Biology, Amyloid beta-Protein Precursor, Mice, β amyloid, Alzheimer Disease, Internal medicine, mental disorders, medicine, Presenilin-1, Dementia, Animals, Cognitive decline, Prefrontal cortex, Pathological, gamma-Aminobutyric Acid, Amyloid beta-Peptides, Symporters, business.industry, General Medicine, medicine.disease, Disease Models, Animal, Endocrinology, nervous system, Potential biomarkers, GABAergic, business
Abstract

Alzheimer's disease (AD) is a neurodegenerative disorder, which has become the leading cause of dementia cases globally. Synaptic failure is an early pathological feature of AD. However, the cause of synaptic failure in AD, especially the GABAergic synaptic activity remains unclear. Extensive evidence indicates that the presence of soluble amyloid-β is an early pathological feature in AD, which triggers synaptic dysfunction and cognitive decline. Our recent study explored the relation of GABAergic transmission and soluble Aβ in early APP/PS1 mice. Firstly, we found soluble Aβ42 levels were significantly increased in serum, hippocampus and prefrontal cortex in 3-4 months APP/PS1 mice, which was much earlier than Aβ plagues formation. In addition, we found TNF-α and BDNF expression levels were increased, while KCC2 and GABAAR expression were decreased in 3-4 months APP/PS1 hippocampus. When we treated 3-4 months APP/PS1 mice with a potent γ-secretase inhibitor, LY411575, which can reduce the soluble Aβ42 levels, the TNF-α and BDNF protein levels were decreased, while KCC2 and GABAAR levels were increased. In conclusion, our study suggested soluble Aβ may impaired the GABA inhibition by mediating KCC2 levels in early APP/PS1 mice. KCC2 may be served as a potential biomarker for AD.

Published
2021

2. Shufengjiedu capsules protect against neuronal loss in olfactory epithelium and lung injury by enhancing autophagy in rats with allergic rhinitis

Author

Hua Kong, Jinyu Mei, Ziyu Chen, Yatang Wang, Zhentao Zhao, and Jianming Yang

Subjects
Male, Pathology, medicine.medical_specialty, Health (social science), Blotting, Western, Interleukin-1beta, H&E stain, Inflammation, Apoptosis, Enzyme-Linked Immunosorbent Assay, Lung injury, Immunoglobulin E, General Biochemistry, Genetics and Molecular Biology, Proinflammatory cytokine, Rats, Sprague-Dawley, 03 medical and health sciences, Random Allocation, 0302 clinical medicine, medicine, Autophagy, Animals, Lung, biology, business.industry, Tumor Necrosis Factor-alpha, General Medicine, Lung Injury, Immunohistochemistry, Rhinitis, Allergic, Rats, Disease Models, Animal, medicine.anatomical_structure, 030220 oncology & carcinogenesis, biology.protein, 030211 gastroenterology & hepatology, Tumor necrosis factor alpha, medicine.symptom, business, Drugs, Chinese Herbal
Abstract

Shufengjiedu capsules (SFJDCs), a traditional Chinese medicine, have been widely used as an antiviral, antibacterial, antitumor, and anti-inflammatory drug. However, the roles of SFJDCs in allergic rhinitis remain unclear. The purpose of this study was to investigate the effects of SFJDCs in olfaction and lung injury in rats with allergic rhinitis. An animal model of allergic rhinitis was created by intraperitoneal injection and intranasal administration of ovalbumin to rats. All rats were divided into seven groups: a model group, a low-dose SFJDC group, a medium-dose SFJDC group, a high-dose SFJDC group, a cetirizine group, and a control group. Hematoxylin and eosin (HE) staining was used to observe pathological changes in rat lung and olfactory epithelium (OE) tissue, and peripheral blood was collected and subjected to an enzyme-linked immunosorbent assay (ELISA) to detect IgE, tumor necrosis factor alpha (TNF-α), and IL-1ꞵ levels. Western blotting, immunohistochemistry staining, and immunofluorescence staining were performed to detect inflammatory cytokines and levels of the autophagy biomarker beclin1 and the apoptosis biomarker cleaeved-caspased3 in lung and OE tissue. ELISA indicated that SFJDCs significantly decreased IgE, TNF-α, and IL-1ꞵ levels in peripheral blood, the lungs, and OE tissue. In addition, Western blotting and staining indicated that SFJDCs repair lung injury, protect against neuronal apoptosis in OE, and rescue impaired autophagy in the lungs and OE tissue. In conclusion, results indicated that SFJDCs might protect against neuronal loss in the OE and lung injury by enhancing autophagy and decreasing apoptosis in rats with allergic rhinitis. Therefore, SFJDCs might serve as an alternative treatment for allergic rhinitis.

Published
2019

3. Shufengjiedu capsules protect against neuronal loss in olfactory epithelium and lung injury by enhancing autophagy in rats with allergic rhinitis.

Author

Jinyu Mei, Hua Kong, Zhentao Zhao, Ziyu Chen, Yatang Wang, and Jianming Yang

Subjects
*ALLERGIC rhinitis, *LUNG injuries, *TUMOR necrosis factors, *ENZYME-linked immunosorbent assay, *IMMUNOGLOBULIN E, *CHINESE medicine, *NASAL mucosa
Abstract

Shufengjiedu capsules (SFJDCs), a traditional Chinese medicine, have been widely used as an antiviral, antibacterial, antitumor, and anti-inflammatory drug. However, the roles of SFJDCs in allergic rhinitis remain unclear. The purpose of this study was to investigate the effects of SFJDCs in olfaction and lung injury in rats with allergic rhinitis. An animal model of allergic rhinitis was created by intraperitoneal injection and intranasal administration of ovalbumin to rats. All rats were divided into seven groups: a model group, a low-dose SFJDC group, a medium-dose SFJDC group, a high-dose SFJDC group, a cetirizine group, and a control group. Hematoxylin and eosin (HE) staining was used to observe pathological changes in rat lung and olfactory epithelium (OE) tissue, and peripheral blood was collected and subjected to an enzyme-linked immunosorbent assay (ELISA) to detect IgE, tumor necrosis factor alpha (TNF-a), and IL-1? levels. Western blotting, immunohistochemistry staining, and immunofluorescence staining were performed to detect inflammatory cytokines and levels of the autophagy biomarker beclin1 and the apoptosis biomarker cleaeved-caspased3 in lung and OE tissue. ELISA indicated that SFJDCs significantly decreased IgE, TNF-a, and IL-1? levels in peripheral blood, the lungs, and OE tissue. In addition, Western blotting and staining indicated that SFJDCs repair lung injury, protect against neuronal apoptosis in OE, and rescue impaired autophagy in the lungs and OE tissue. In conclusion, results indicated that SFJDCs might protect against neuronal loss in the OE and lung injury by enhancing autophagy and decreasing apoptosis in rats with allergic rhinitis. Therefore, SFJDCs might serve as an alternative treatment for allergic rhinitis. [ABSTRACT FROM AUTHOR]

Published
2019
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4. Soluble ß-amyloid impaired the GABA inhibition by mediating KCC2 in early APP/PS1 mice.

Author

Yuan Zhou, Yujie Cheng, Yong Li, Jiyao Ma, Zhihan Wu, Yuenan Chen, Jinyu Mei, and Ming Chen

Subjects
*AMYLOID beta-protein precursor, *GABA, *COGNITION disorders, *PLAGUE, *ALZHEIMER'S disease, *MICE, *PREFRONTAL cortex, *MOBILE apps
Abstract

Alzheimer's disease (AD) is a neurodegenerative disorder, which has become the leading cause of dementia cases globally. Synaptic failure is an early pathological feature of AD. However, the cause of synaptic failure in AD, especially the GABAergic synaptic activity remains unclear. Extensive evidence indicates that the presence of soluble amyloid-ß is an early pathological feature in AD, which triggers synaptic dysfunction and cognitive decline. Our recent study explored the relation of GABAergic transmission and soluble Aß in early APP/PS1 mice. Firstly, we found soluble Aß42 levels were significantly increased in serum, hippocampus and prefrontal cortex in 3-4 months APP/PS1 mice, which was much earlier than Aß plagues formation. In addition, we found TNF-a and BDNF expression levels were increased, while KCC2 and GABAAR expression were decreased in 3-4 months APP/PS1 hippocampus. When we treated 3-4 months APP/PS1 mice with a potent ?-secretase inhibitor, LY411575, which can reduce the soluble Aß42 levels, the TNF-a and BDNF protein levels were decreased, while KCC2 and GABAAR levels were increased. In conclusion, our study suggested soluble Aß may impaired the GABA inhibition by mediating KCC2 levels in early APP/PS1 mice. KCC2 may be served as a potential biomarker for AD. [ABSTRACT FROM AUTHOR]

Published
2021
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