INFLAMMOPHARMACOLOGY
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2024
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IF 4.6
Weng Jiyu,Wang Ying,Tan Zekai,Yuan Yanghe,Huang Shiyuan,Li Zexi,Li Yiming,Zhang Lanyue,Du Zhiyun
Objectives Chronic neuroinflammation has become one of the important causes of common neurodegeneration disease. Therefore, the target of this study was to explore the protective action of glabridin on lipopolysaccharide (LPS)-induced neuroinflammation in vivo and in vitro and its mechanism. Methods The neuroinflammation model was established by LPS-induced BV2 cells. The cell viability with various concentrations of glabridin was determined by MTT assay, and the content of NO in each group was detected. A neuroinflammatory model was established in male C57BL/6J mice for a water maze test. Subsequently, NF-κB and SOD indices were measured by ELISA, GFAP and IBA-1 indices were measured by immunofluorescence, and Nissl staining was used to explore the Nissl bodies in the hippocampus of mice. Results In vitro experiments, our results expressed that glabridin could markedly increase the cell activity of LPS-induced BV2 cells and reduce the NO expression in cells. It indicated that glabridin had a remarkable impact on the neuroinflammation of LPS-induced BV2 cell protection. In vivo neuroinflammation experiments, mice treated with different doses of glabridin showed significantly improved ability of memory compared with the LPS group in the Morris water maze test. The levels of NF-κB, GFAP, and the number of positive cells in Nissl staining were decreased. High-dose glabridin significantly increased the SOD content in the brain tissue and decreased the IBA-1 levels. Conclusion Glabridin can significantly reduce or even reverse LPS-induced neuroinflammation, which may be related to the fact that glabridin can reduce the NO expression, NF-κB, IBA-1, GFAP, and other inflammatory mediators, upregulate the expression of SOD to relieve oxidative stress of brain and inhibit the activation of gliocyte in brain tissue.
研究领域:
神经科学
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药理学
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免疫学
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细胞生物学
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产品关联
DOI
PubMed
高影响因子
Molecular Medicine Reports
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2019
·Vol. 19
·期 4
·2758-2766
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IF 1.851
Ya Hou,Xiaobo Wang,Xiaorui Chen,Jing Zhang,Xiaopeng Ai,Yusheng Liang,Yangyang Yu,Yi Zhang,Xianli Meng,Tingting Kuang,Yao Hu
This study was conducted to establish a stable hypobaric hypoxia brain injury model. SD rats were randomly separated into control and model groups, and placed outside or inside of a hypobaric chamber, respectively. Subsequent to 24 h anoxic exposure, plasma superoxide dismutase (SOD), malondialdehyde (MDA), glutathione (GSH), oxidized glutathione (GSSG) and lactate dehydrogenase (LDH) were measured using commercial biochemical kits. Hematoxylin‑eosin (H&E), Nissl's and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining were used to observe the morphology of neurons in the hippocampus. The protein expression levels of apoptotic protease activating factor‑1 (Apaf‑1), hypoxia inducible factor‑1α (HIF‑1α), caspase‑3, cleaved caspase‑3, Bcl‑2‑associated X protein (Bax) and cytochrome c (cyto‑c) were detected using western blot and immunohistochemistry analyses. Hypoxic substantially induced morphological lesions in the hippocampus concomitant with the physical behavioral performance deficit. Furthermore, hypoxia markedly exacerbated the levels of MDA, LDH and GSSG, and restrained GSH (P<0.01) and SOD (P<0.05) levels compared with the control group. In addition, hypoxia significantly induced the protein expression of Apaf‑1, HIF‑1α, caspase‑3, cleaved caspase‑3, Bax and Cyto‑c (P<0.01) compared with the control group. Finally, a lower number and volume of Nissl bodies were verified in the hypoxic group. TUNEL results demonstrated a greater number of apoptotic cells in the hypoxic group. The present study demonstrates a model of rat hypoxic brain injuries induced by a hypobaric chamber at 9,000 m for 24 h. Furthermore, the redox enzyme, HIF‑1α and mitochondrial apoptosis‑associated protein, along with H&E and Nissl's staining, may be applied to evaluate the degree of injury.
研究领域:
神经科学
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药理学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
NEUROTOXICOLOGY
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2023
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IF 3.4
Tong Zhang,Chunmei Zhang,Yuyou Luo,Shuping Liu,Siyuan Li,Lixia Li,Yuxin Ma,Jing Liu
The present study aimed to investigate the protective effect of rutin on the injury of spinal motor neuron in rats exposed to acrylamide (ACR) the underlying mechanism. Fifty male Sprague-Dawley rats, aged 7–8 weeks, were randomly divided into control group, ACR group (20 mg/kg), low dose(100 mg/kg), medium dose (200 mg/kg) and high dose(400 mg/kg) rutin groups, ten rats in each group. The rats were given intragastric administration for 21 days. Every week, a neurobehavioral test was conducted. Nissl staining was used to observe the morphological changes in motor neurons in the L4-L6 segment of the spinal cord . Immunohistochemistry was used to identify AChE and ChAT in the rat spinal cord. Western blot was used to identify the expression of AChE, ChAT, P-ERK, ERK, and Nrf2 proteins in the rat spinal cord. The commercial kits were used to detect the presence of SOD, GSH, and LDH in the rat spinal cord. At the start of the second week, the medium and high dosage rutin group's rats' gait scores significantly decreased as compared to those of the ACR group. When rutin dosage was increased, the Nissl staining revealed that Nissl bodies was staining intensified compared to the ACR group. Immunohistochemistry and Western blot analysis revealed that AChE and ChAT expression changed when rutin dose was raised, but P-ERK and Nrf2 expression steadily increased in the spinal cord of rats in the medium and high dose groups compared to the ACR group. In the spinal cord of rats in each dosage group compared to the ACR group, the findings of the oxidative stress indices demonstrated that the expression levels of SOD and GSH rose with the increase of rutin dose, while the expression of LDH reduced with the rise of rutin dose. Rutin has an anti-oxidative impact through up-regulating the expression of P-ERK and Nrf2 proteins in the ERK/Nrf2 pathway, which may be connected to its protective action on motor neurons in the spinal cord of rats exposed to ACR.
研究领域:
神经科学
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药理学
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毒理学
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产品关联
DOI
PubMed
高影响因子
JOURNAL OF THE SCIENCE OF FOOD AND AGRICULTURE
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2025
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IF 3.5
Siqi Shen,Songyi Lin,Deyou Gao,Jianlan Hu,Zhijie Bao
BACKGROUND Memory impairment, a hallmark manifestation of neurodegenerative disorders exemplified by Alzheimer's disease, constitutes a critical global public health challenge requiring urgent therapeutic innovation. The present study aims to systematically investigate the potential mechanisms of fish scale collagen peptides (FSCP) in enhancing cognitive function through behavioral experiments, detection of hippocampal biochemical indicators and histopathological observation. Concurrently, liquid chromatography-tandem mass spectrometry analysis and in silico methods were utilized to screen active peptide fragments with potential auxiliary effects on memory improvement. RESULTS The results of our study demonstrated that mice treated with a medium dose of FSCP via gavage exhibited optimal behavioral performance. Moreover, the number of Nissl bodies in the CA1 and CA3 regions increased to (114.83 ± 8.74) and (71.67 ± 5.79), respectively. Hippocampal pathology was improved, Acetylcholine levels were elevated, Acetylcholinesterase ctivity was decreased and hippocampal oxidative stress was reduced in the mice. Among the digested products of FSCP, the tripeptides PPP, GGL, GLL and MAP were found to exhibit higher relative abundance and activity scores. CONCLUSION These results demonstrate that mice treated with a medium dose of FSCP via gavage exhibited the most substantial improvement in memory function. Bioactive peptides such as PPP and GGL are promising to provide a new source for the development of drugs for assisted memory improvement. © 2025 Society of Chemical Industry.
研究领域:
神经科学
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药理学
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生物化学
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分子生物学
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神经退行性疾病
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肽类研究
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认知科学
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产品关联
DOI
PubMed
高影响因子
Biomaterials Advances
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2023
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IF 0
Xiaoyu Xia,Han Li,Xianbing Xu,Chao Wu,Zhenyu Wang,Junjie Yi,Guanghua Zhao,Ming Du
Recombinant human H-ferritin nanocage (rHuHF) loaded with natural antioxidative lycopene molecules (LYC) was successfully constructed for the first time, aiming to enrich LYC in the brain and explore the regulation mechanism of this nanoparticles on neurodegeneration. Here, the mouse model was constructed via D-galactose-induced neurodegeneration based on behavioural analysis, histological observation, immunostaining analysis, Fourier transform infrared microscopy, and Western blotting analysis for the regulation of rHuHF-LYC. rHuHF-LYC improved the behaviour of mice in a dose-dependent manner. Besides, rHuHF-LYC can attenuate neuronal damage, maintain the number of Nissl body, increase the level of unsaturated fat, inhibit the activation of glial cells, and prevent excessive accumulation of neurotoxic proteins in the hippocampus of mice. More importantly, synaptic plasticity was activated in response to the regulation of rHuHF-LYC with excellent biocompatibility and biosafety. This study proved the validity of the direct use of natural antioxidant nano drugs for treating neurodegeneration, providing a promising therapeutic option against further imbalances in the degenerative brain microenvironment.
研究领域:
神经科学
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药学
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生物技术
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分子生物学
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产品关联
DOI
PubMed
Bioactive Materials
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2020
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IF 8.724
Yantao Zheng,Gang Wu,Limei Chen,Ying Zhang,Yuwei Luo,Yong Zheng,Fengjun Hu,Tymor Forouzanfar,Haiyan Lin,Bin Liu
Brain tissues that are severely damaged by traumatic brain injury (TBI) is hardly regenerated, which leads to a cavity or a repair with glial scarring. Stem-cell therapy is one viable option to treat TBI-caused brain tissue damage, whose use is, whereas, limited by the low survival rate and differentiation efficiency of stem cells. To approach this problem, we developed an injectable hydrogel using imidazole groups-modified gelatin methacrylate (GelMA-imid). In addition, polydopamine (PDA) nanoparticles were used as carrier for stromal-cell derived factor-1 (SDF-1α). GelMA-imid hydrogel loaded with [email protected] α nanoparticles and human amniotic mesenchymal stromal cells (hAMSCs) were injected into the damaged area in an in-vivo cryogenic injury model in rats. The hydrogel had low module and its average pore size was 204.61 ± 41.41 nm, which were suitable for the migration, proliferation and differentiation of stem cells. In-vitro cell scratch and differentiation assays showed that the imidazole groups and SDF-1α could promote the migration of hAMSCs to injury site and their differentiation into nerve cells. The highest amount of nissl body was detected in the group of GelMA-imid/SDF-1α/hAMSCs hydrogel in the in-vivo model. Additionally, histological analysis showed that GelMA-imid/SDF-1α/hAMSCs hydrogel could facilitate the regeneration of regenerate endogenous nerve cells. In summary, the GelMA-imid/SDF-1α/hAMSCs hydrogel promoted homing and differentiation of hAMSCs into nerve cells, and showed great application potential for the physiological recovery of TBI.
研究领域:
神经科学
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干细胞疗法
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生物材料
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再生医学
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DOI
PubMed
高影响因子
JOURNAL OF SURGICAL RESEARCH
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2021
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IF 2.192
Wenjun Zheng,Bing Liu,Enyi Shi
ABSTRACT Background Spinal Cord ischemia-reperfusion injury (SCII) is one of the most destructive complications in thoracic-abdominal aortic surgery, which can cause physical abnormalities, paralysis and even brain death. Evidence has shown that perillaldehyde (PAH) can ameliorate rat's cerebra ischemia-reperfusion injury. However, the effect of PAH on SCII remains unknown. Methods The current study established SCII rat models and oxygen and glucose deprivation/reoxygenation-induced BV2 microglia models to explore whether PAH could alleviate SCII symptoms and to investigate underlying mechanism. Results SCII rats underwent severe neurologic motor dysfunction and histopathologic injury compared with the normal rats, which are exhibited by loss of motor neurons and decrease of nissl bodies . Treatment with PAH significantly ameliorated motor dysfunction and neuron damage. PAH downregulated the expression of NLR family pyrin domain containing 3 , cleaved/pro caspase-1, interleukin-1β and interleukin-18 in spinal cord tissues of SCII rats. Besides, the contents of oxidative stress-related factors superoxide dismutase, manganese-dependent superoxide dismutase, catalase and glutathione peroxidase were significantly increased and malondialdehyde content was decreased after PAH treatment. PAH treatment upregulated the expression of nuclear factor-E2-related factor 2 and heme oxygenase-1 in spinal cord tissues of SCII rats. Our in vitro study confirmed that PAH inhibited microglial activation by activating the nuclear factor-E2-related factor 2/heme oxygenase-1 pathway, exhibited by alleviated inflammation and oxidative stress . Conclusions This study elucidates that PAH has the potential value for treating SCII, which provides an experimental basis for clinical trials in the future.
研究领域:
神经科学
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药理学
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分子生物学
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病理生理学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
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