Food Bioscience
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2023
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IF 5.2
Jiaxin Li,Hengju Ge,Yang Xu,Jiahong Xie,Naymul Karim,Fujie Yan,Jianling Mo,Wei Chen
Chlorogenic acid (CGA) is a phenylpropanoid compound in chrysanthemum, which has a variety of biological activities. Nevertheless, CGA has not yet been studied concerning oxidative stress in hepatocytes. Our research aims to investigate whether chlorogenic acid can improve hepatic oxidative stress, and further illustrated its detailed mechanism. The results of free radicals measurement and Western blot showed that CGA suppressed the activation of JNK (c-Jun NH2-teminal kinase) signaling pathway by ameliorating endoplasmic reticulum stress in H 2 O 2 -treated hepatocytes, thereby eliminating excess intracellular free radicals. In addition, through RT-qPCR, we found that miR-199a-5p down-regulated in H 2 O 2 -induced L02 cells, which was restored by CGA. By inhibiting the expression of miR-199a-5p to promote the transcription of GRP78 gene, the antioxidant capacity of CGA was greatly weakened in hepatocytes. Our findings suggest that CGA treatment alleviated the H 2 O 2 -induced oxidative stress by targeting miR-199a-5p, thereby ameliorating ER stress and inhibiting JNK phosphorylation for antioxidant capacity enhancement. Based on our available results, CGA may be an alternative compound to mitigate hepatic oxidative damage through the miR-199a-5p/GPR78 axis.
研究领域:
药理学
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分子生物学
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细胞生物学
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DOI
高影响因子
MATERIALS TECHNOLOGY
·
2024
·
IF 2.9
Mengcheng Xu,Maolin Zhao
Among deaths related to cardiovascular disease (CVD), arteriosclerosis accounts for three-quarters of the total. The most common treatment for arteriosclerosis is revascularization through the implantation of endovascular scaffolds. However, most metal scaffolds currently available are non-biodegradable, which can lead to rejection reactions. In this study, we have developed a CMCS-PEI/miR polysaccharide nucleic acid nanodrug loaded with miR-199a-5p for the first time. The CMCS-PEI/miR polysaccharide nucleic acid nanodrug exhibits good blood compatibility, successfully transfects cells, and induces apoptosis of vascular endothelial cells. Additionally, PCL/GO composite scaffolds with excellent mechanical properties and biocompatibility were fabricated using 3D printing technology. This technology allows for the customisation of scaffolds to meet the needs of individual patients. The 3D-printed PCL/GO composite scaffolds loaded with CMCS-PEI/miRNA polysaccharide nucleic acid nanodrug effectively induce apoptosis of vascular endothelial cells, showing great potential in promoting the functional repair of arteriosclerosis and preventing vascular restenosis.
研究领域:
心血管疾病
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生物材料学
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分子生物学
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组织工程
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DOI
高影响因子
Oxidative Medicine and Cellular Longevity
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2022
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IF 7.31
Hongshu Wang,Xianyi Wang,Xiaomin Liu,Jinbao Zhou,Qianqian Yang,Binshu Chai,Yimin Chai,Zhongliang Ma,Shengdi Lu
Diabetes mellitus (DM) is a growing health problem. As a common complication of DM, diabetic foot ulcer (DFU) results in delayed wound healing and is a leading cause of nontraumatic amputation. miR-199a-5p, a short noncoding RNA, had abnormal expression in DFU wound tissues. The expression of miR-199a-5p was significantly increased in DFU wound tissues, skin tissues of diabetic rats, and high glucose-induced cells. Vascular endothelial growth factor A (VEGFA) and Rho-associated kinase 1 (ROCK1) are directly targets of miR-199a-5p. Inhibiting the expression of miR-199a-5p alleviated the inhibition of VEGFA and ROCK1, thereby rescued impaired proliferation and migration of HG-induced cells, and restored the normal function of the cells to some extent. In diabetic rats, inhibition of miR-199a-5p significantly increased the expression of VEGFA and ROCK1, significantly promoted wound healing, and rescued impaired wound healing. miR-199a-5p and its targets showed therapeutic effect on diabetic wounds.
研究领域:
分子生物学
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内分泌学
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伤口愈合
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糖尿病研究
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DOI
PubMed
高影响因子
Scientific Reports
·
2025
·Vol. 15
·期 1
·44020
·
IF 3.9
Li Zhipeng,Liu Zhaoheng,Wei Wan,Niu Jie,Wu Jianjun,Jiao Yang
This study explored the therapeutic potential of Number 2 Feibi Recipe (FBR2), a traditional Chinese medicine prescription, in the treatment of idiopathic pulmonary fibrosis (IPF). Specifically, it investigated whether FBR2 mediated its effects by modulating miR-199a-5p expression, activating the SIRT1/AMPK/mTOR pathway and then promoting autophagy. Eighty-four mice were divided into seven groups: Control, bleomycin (BLM), FBR2, self-complementary adeno-associated virus expressing miR-199a-5p (scAAV-miR-199a-5p), scAAV-negative control (scAAV-NC), FBR2 + BLM + scAAV-miR-199a-5p, and FBR2 + BLM + scAAV-NC. Fluorescence staining, miR-199a-5p expression levels, histopathological changes, protein expression and autophagy activity were assessed using various techniques, including RT-qPCR, histopathological staining, Western blotting, Elisa and transmission electron microscopy (TEM). FBR2 treatment significantly reduced miR-199a-5p expression elevated by BLM and improved histopathology, reduced levels of α-smooth muscle actin (α-SMA) and collagen-III, and increased E-cadherin expression. FBR2 also enhanced autophagy, as evidenced by elevated LC3-II and Beclin-1 levels and reduced p62 expression. Additionally, it activated the SIRT1/AMPK/mTOR pathway. Finally, network pharmacology identified 227 compounds in FBR2, among which Kaempferol and Quercetin (two major shared constituents) showed strong binding to miR-199a-5p in molecular docking, suggesting their potential as key active components. This study showed FBR2 attenuated BLM-induced pulmonary fibrosis in mice by reducing miR-199a-5p expression and promoting autophagy which may be achieved by modulating the SIRT1/AMPK/mTOR pathway. These findings provide novel insights into the mechanism of FBR2 and its potential as a therapeutic approach for IPF.
研究领域:
药理学
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中医
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分子生物学
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呼吸系统疾病研究
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自噬信号通路
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DOI
PubMed
高影响因子
INTERNATIONAL IMMUNOPHARMACOLOGY
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2025
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IF 4.7
Lanxi Xu,Yan Feng,Xintian Zheng,Meiyu Wang,Yan Fang,Lin Li,Jiadong Xu,Yani Zhang,Weiru Jiang,Lisheng Chu
Neuronal loss following ischemic stroke (IS) is a major cause of long-term neurological dysfunction. Neural stem cell (NSC) transplantation holds great potential for neural tissue repair, but exogenous NSCs often over-differentiate into astrocytes, resulting in glial scar formation and poor neuronal maturation, which limits clinical application. Astragaloside IV (AS-IV), a plant-derived monomer, has been shown to regulate the proliferation, migration, and differentiation of endogenous NSCs. This study investigated whether AS-IV preconditioning could promote the neurogenesis of transplanted NSCs and improve functional recovery after IS. Primary NSCs were cultured and exposed to various concentrations of AS-IV, and 100 μM was selected for further use. A rat model of middle cerebral artery occlusion/reperfusion (MCAO/R) was established, and AS-IV-preconditioned or untreated EGFP-labeled NSCs were transplanted into the striatum. Brain injury was assessed histologically. Neurological recovery was evaluated using the modified Neurological Severity Score, grip strength, adhesive removal, and Morris water maze tests. Immunofluorescence staining was used to assess graft survival, differentiation fate, synapse formation, and glial scar area. In vitro experiments explored the involvement of the miR-199a-5p/Caveolin-1 signaling pathway. AS-IV preconditioning significantly improved the survival and neuronal differentiation of grafted NSCs, reduced astrocytic lineage commitment and glial scar formation, and enhanced synaptic reconstruction. These effects were associated with improved sensorimotor and cognitive function. In conclusion, AS-IV pretreatment of NSCs promoted neuronal lineage commitment, inhibited glial scarring, and facilitated functional recovery after ischemic stroke. Targeting the miR-199a-5p/Caveolin-1 axis may offer a novel strategy for optimizing NSC-based therapy in stroke.
研究领域:
神经科学
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干细胞治疗
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分子生物学
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再生医学
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脑血管疾病
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DOI
PubMed
高影响因子
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