CARBOHYDRATE POLYMERS
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2023
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IF 11.2
Jing Wen,Chang Liu,Ji Liu,Lu Wang,Si Miao,Daquan Chen,Qiyue Wang,Meirong Huo,Yan Shen
At present, NIR-II-triggered photothermal biomedical applications are limited by complex synthesis reactions , mediocre photothermal conversion efficiency, and difficult degradation. Herein, we prepared biodegradable Bi flower-like nanoparticles (phospholipid-modified Bi nanoflowers , BNFs) with high photothermal conversion efficiency (∼33.52 %) in NIR-II by a simple method and then modified them with the red blood cell membrane and dextran 40 (DRBCM) to improve their in vitro stability, to escape macrophages clearance and to enhance tumor accumulation. Dextran coating onto the surface of particles as a dispersant shell stabilizes inorganic particles by maintaining the surface charges and creating steric repulsions upon compression of neighboring polymer chains. In vitro and in vivo experiments proved that combined thermoradiotherapy of DRBCM-BNFs exhibited significantly enhanced tumor inhibition efficacy than monotherapy with good biocompatibility and low toxicity due to its biodegradability . Furthermore, the mechanism studies demonstrated that DRBCM-BNFs could serve as a nano sensitizer to promote the thermoradiotherapy under NIR-II illumination and X-ray irradiation, by downregulating heat shock protein 70 (HSP70) and phosphorylated-p65 (p-p65) to reduce the thermal resistance and radioresistance of tumor cells and increasing the expression of apoptosis-related protein cleaved caspase-3. In conclusion, DRBCM-BNFs could be a promising green delivery platform for the sensitization of synergistic thermoradiotherapy.
研究领域:
纳米技术
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生物医学工程
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癌症治疗
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材料科学
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生物物理学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Food Bioscience
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2024
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IF 4.8
Yusi Qin,Ning Wang,Xinlu Yuan,Juanjuan Luo,Junnan Wan,Yiting Zhao,Cunfang Wang,Xiaoning Zhang
This work investigated the protective effects of high Fischer's ratio oligopeptides from goat ( Capra hircus ) whey protein (HFO) against CCl 4 -induced acute liver injury in vivo and their underlying mechanism of action. The results showed that HFO inhibited the rise of serum transaminases (including alanine aminotransferase and aspartate aminotransferase), leading to an increase in the levels of superoxide dismutase and glutathione peroxidase and inhibition of malondialdehyde content, thus ameliorating the CCl 4 -induced liver lesions. Moreover, the levels of cytokines, tumor necrosis factor-α, interleukin-6, and interleukin-1β decreased significantly, indicating that HFO alleviates the CCl 4 -induced inflammatory response by reducing the levels of inflammatory factors in mice. Additionally, Western blot analysis showed that HFO treatment significantly promoted the expression of IkappaB-alpha antibody and inhibited the expression of phosphorylated p65, suggesting that the anti-inflammatory activity is one of the reasons for the hepatoprotective effects of HFO. In conclusion, HFO can potentially be used as a component of functional foods with a particular focus on treating chemical liver injury.
研究领域:
药理学
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毒理学
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免疫学
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生物化学
✓ 已验证
产品关联
DOI
高影响因子
Journal of Inflammation Research
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2021
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IF 6.922
Zhen-Hua Ying,Hui-Min Li,Wen-Ying Yu,Chen-Huan Yu
Purpose Abnormal glycolysis of immune cells contributed to the development of inflammatory response. Inhibition of this Warburg phenotype could be a promising strategy for preventing various inflammatory diseases. Iridin (IRD) is a natural isoflavone, and exerts anticancer, antioxidant, and anti-inflammatory effects. However, the underlying mechanism of IRD on acute inflammation remains unknown. In this study, the protective effects of IRD against lipopolysaccharide (LPS)-induced inflammation were investigated in murine macrophage RAW264.7 cells and in mice. Methods The inhibition of IRD on NO production in culture medium was detected by Griess assay while the levels of TNF-α, IL-1β, and MCP-1 were detected by ELISA assay. The effects of IRD on OCR and ECAR levels in LPS-treated macrophages were monitored by using Seahorse Analyzer. The apoptosis rate as well as the release of ROS and NO of RAW264.7 cells were analyzed by flow cytometric assay. The protective effects of IRD were investigated on LPS-induced inflammation in mice. The expressions of PKM2 and its downstream (p-JAK1, p-STAT1, p-STAT3, p-p65, iNOS, and COX2) in cells and in lung tissues were detected by Western blotting analysis. Results IRD treatment at the concentrations of 12.5–50 μM significantly inhibited the productions of TNF-α, IL-1β, MCP-1, and ROS, and suppressed the levels of glucose uptake and lactic acid in LPS-treated RAW264.7 cells. Oral administration with IRD (20–80 mg/kg) inhibited LPS-induced acute lung injury as well as inflammatory cytokine production in mice. Moreover, IRD targeted pyruvate kinase isozyme type M2 (PKM2) and suppressed its downstream p-JAK1, p-STAT1, p-STAT3, p-p65, iNOS, and COX2, which could be abolished by PKM2 agonist DASA-58 and antioxidant N-acetyl-L-cysteine, but partly be reversed by NF-κB activator CUT129 and JAK1 activator RO8191. Conclusion IRD alleviated LPS-induced inflammation through suppressing PKM2-mediated pathways, and could be a potential candidate for the prevention of inflammatory diseases.
研究领域:
药理学
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免疫学
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细胞生物学
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分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
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