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RSC96细胞
POLYMER INTERNATIONAL · 2022 ·Vol. 71 ·期 8 ·1022-1029 · IF 3.213

Development of a novel vector for siRNA delivery based on arginine-modified polyvinylamine

Mei Lin,Aizhu Lin,Sheng Huang,Tianhui Liu,Fang Ke,Deshun Qiu,Xuefeng Lin,Daoshu Luo

An ideal carrier that delivers small interfering RNA (siRNA) should be designed based on two criteria: high gene transfection efficiency and low cytotoxicity. In this work, arginine was used to modify polyvinylamine (PVAm) to form a novel PVAm derivative (PVAm-Arg) for siRNA delivery and the derivative was characterized using Fourier transform infrared spectroscopy. PVAm-Arg/siRNA complexes were formed by the self-assembly method. The zeta potential and size of the complexes were measured using electrophoretic light scattering and dynamic light scattering, respectively. The siRNA binding capacity of PVAm-Arg was assessed using gel retardation assay. The results showed that PVAm-Arg derivatives can bind siRNA effectively and form complexes with sizes of about 72 ± 2 nm. What is more, the ability of PVAm-Arg to condense siRNA was better than that of PVAm. Cytotoxicity assay with RSC96 cells also showed that PVAm-Arg had lower cytotoxicity compared with PVAm. In in vitro cellular uptake assay, PVAm-Arg showed good transfection efficiency. Therefore, we concluded that PVAm-Arg would be a promising candidate as a gene delivery vector. © 2022 Society of Industrial Chemistry.

CAS / MDL: 25952-53-8
研究领域: 生物技术 · 药学 · 分子生物学
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BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS · 2024 · IF 2.5

Low expression of Frataxin might contribute to diabetic peripheral neuropathy in a mouse model

Siyu Xia,Lin Wu,Jing Chen,Kuanyu Li,Dezhi Bian

Diabetes is one of the most prevalent metabolic disorders, and its incidence has been experiencing a steady annual rise in recent years. Diabetic peripheral neuropathy (DPN) represents the most frequent adverse complication, exerting a profound impact on the quality of life for those suffering from diabetes. The etiology of DPN is complex, including impaired mitochondrial function. Iron-sulfur clusters (Fe–S) are essential cofactors for numerous essential enzymes crucial for mitochondrial function. Our previous study showed that expression of Frataxin, encoded by the Fxn gene, is downregulated in leptin receptor knockout (so-called db/db) mice, a commonly used DPN mouse model. Fxn is one of the core components of Fe–S biogenesis machinery. Here, we found that the mitochondria-targeted antioxidant SS-31 markedly improved the behavioral indices and significantly mitigated the damage to the sciatic nerve. SS-31 treatment effectively elevated Fxn expression, meliorated mitochondrial function, and inflammation in the sciatic nerve (SCN). We also found that SS-31 effectively mitigated high glucose-induced disruption of iron and redox homeostasis in RSC96 cells, a typical cell model of DPN, thereby improving mitochondrial function. These findings suggest enhancing Fe–S biogenesis could be an effective therapeutic strategy for treating DPN.

CAS / MDL: 148504-34-1
研究领域: 代谢性疾病 · 神经科学 · 分子生物学 · 糖尿病研究
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International Journal of Polymeric Materials and Polymeric Biomaterials · 2023 · IF 3.2

Electrospun SF/GO/VEGF/GAS-LP scaffolds with synergistic sequential drug release and electrical stimulation for accelerated peripheral nerve regeneration

Jiashuo Liu,Runzhi Xiang,Hongtao Li,Hong Zhu,Jiarui Dang,Zhihui Ran,Huan Deng,Wenjin Xu,Chengjie Xiong,Zhijun Huang,Peihu Xu,Haixing Xu

Here, a novel kind of composite scaffold was fabricated by loading vascular endothelial growth factor (VEGF) and gastrodin liposome (GAS-LP) into electrospun silk fibroin/graphene oxide(SF/GO)nanofibrous and silk fibroin sponge-filled, respectively. Our results demonstrated that VEGF and GAS exhibited different release patterns in vitro which VEGF showed rapid release rate in the first few days while GAS was released slowly and continuously as encapsulated in liposomes. The scaffolds realized the combination of intraneural vascularization drugs and electrical stimulation effectively, leading to enhanced growth of RSC96 cells. Furthermore, the scaffolds could protect RSC96 cells in an inflammatory environment.

CAS / MDL: 57-88-5 8002-43-5
研究领域: 生物材料 · 组织工程 · 神经科学 · 药物递送系统
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CNS Neuroscience & Therapeutics · 2023 ·Vol. 29 ·期 4 ·1000-1011 · IF 5.5

Ferulic acid alleviates sciatica by inhibiting neuroinflammation and promoting nerve repair via the TLR4/NF-κB pathway

Di Zhang,Bei Jing,Zhen-ni Chen,Xin Li,Hui-mei Shi,Ya-chun Zheng,Shi-quan Chang,Li Gao,Guo-ping Zhao

Introduction Sciatica causes intense pain. No satisfactory therapeutic drugs exist to treat sciatica. This study aimed to probe the potential mechanism of ferulic acid in sciatica treatment. Methods Thirty-two SD rats were randomly divided into 4 groups: sham operation, chronic constriction injury (CCI), mecobalamin, and ferulic acid. We conducted RNA sequencing, behavioral tests, ELISA, PCR, western blotting, and immunofluorescence analysis. TAK-242 and JSH23 were administered to RSC96 and GMI-R1 cells to explore whether ferulic acid can inhibit apoptosis and alleviate inflammation. Results RNA sequencing showed that TLR4/NF-κB pathway is involved in the mechanism of sciatica. CCI induced cold and mechanical hyperalgesia; destroyed the sciatic nerve structure; increased IL-1β, IL-6, TNF-α, IL-8, and TGF-β protein levels and IL-1β, IL-6, TNF-α, TGF-β, TLR4, and IBA-1 mRNA levels; and decreased IL-10 and INF-γ protein levels and IL-4 mRNA levels. Immunohistochemistry showed that IBA-1, CD32, IL-1β, iNOS, nNOS, COX2, and TLR4 expression was increased while S100β and Arg-1 decreased. CCI increased TLR4, IBA-1, IL-1β, iNOS, Myd88, p-NF-κB, and p-p38MAPK protein levels. Treatment with mecobalamin and ferulic acid reversed these trends. Lipopolysaccharide (LPS) induced RSC96 cell apoptosis by reducing Bcl-2 and Bcl-xl protein and mRNA levels and increasing Bax and Bad mRNA and IL-1β, TLR4, Myd88, p-NF-κB, and p-p38MAPK protein levels, while ferulic acid inhibited cell apoptosis by decreasing IL-1β, TLR4, Myd88, p-NF-κB, and p-p38MAPK levels and increasing Bcl-2 and Bcl-xl levels. In GMI-R1 cells, Ferulic acid attenuated LPS-induced M1 polarization by decreasing the M1 polarization markers IL-1β, IL-6, iNOS, and CD32 and increasing the M2 polarization markers CD206, IL-4, IL-10 and Arg-1. After LPS treatment, IL-1β, iNOS, TLR4, Myd88, p-p38MAPK, and p-NF-κB levels were obviously increased, and Arg-1 expression was reduced, while ferulic acid reversed these changes. Conclusion Ferulic acid can promote injured sciatic nerve repair by reducing neuronal cell apoptosis and inflammatory infiltration though the TLR4/NF-κB pathway.

CAS / MDL: 1135-24-6
研究领域: 神经科学 · 药理学 · 分子生物学 · 细胞生物学 · 炎症研究
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