INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
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2024
·Vol. 25
·期 8
·4276
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IF 4.9
Chenyang Li,Xinxin Qi,Lei Xu,Yuan Sun,Yan Chen,Yuhan Yao,Jun Zhao
This study aimed to investigate the preventive effects of the total polyphenols fromNymphaea candida(NCTP) on LPS-induced septic acute lung injury (ALI) in mice and its mechanisms. NCTP could significantly ameliorate LPS-induced lung tissue pathological injury in mice as well as lung wet/dry ratio and MPO activities (p< 0.05). NCTP could significantly decrease the blood leukocyte, neutrophil, monocyte, basophil, and eosinophil amounts and LPS contents in ALI mice compared with the model group (p< 0.05), improving lymphocyte amounts (p< 0.05). Moreover, compared with the model group, NCTP could decrease lung tissue TNF-α, IL-6, and IL-1β levels (p< 0.05) and downregulate the protein expression of TLR4, MyD88, TRAF6, IKKβ, IκB-α, p-IκB-α, NF-κB p65, p-NF-κB p65, NLRP3, ASC, and Caspase1 in lung tissues (p< 0.05). Furthermore, NCTP could inhibit ileum histopathological injuries, restoring the ileum tight junctions by increasing the expression of ZO-1 and occludin. Simultaneously, NCTP could reverse the gut microbiota disorder, restore the diversity of gut microbiota, increase the relative abundance of Clostridiales and Lachnospiraceae, and enhance the content of SCFAs (acetic acid, propionic acid, and butyric acid) in feces. These results suggested that NCTP has preventive effects on septic ALI, and its mechanism is related to the regulation of gut microbiota, SCFA metabolism, and the TLR-4/NF-κB and NLRP3 pathways.
研究领域:
药理学
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免疫学
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微生物学
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病理学
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分子生物学
✓ 已验证
DOI
PubMed
高影响因子
Food & Function
·
2025
·
IF 5.4
Yi-Long Ma,Zhi Li,Qian-Lan Wu,Jing Li,Xin Guo,Tian-Le Mao,Kiran Thakur,Zhao-Jun Wei
3,5-O-Dicaffeoylquinic acid (3,5-DCQA) from edible Gongju chrysanthemum has shown protective effects against alcoholic hepatocyte injury in our previous study. However, the specific effects and mechanisms of 3,5-DCQA in a mouse model of liver injury remain underexplored. This study aimed to examine the efficacy and primary mechanism of 3,5-DCQA from Gongju chrysanthemum in ameliorating acute alcoholic liver injury in mice. The results indicated that 3,5-DCQA effectively attenuated inflammation and apoptosis by regulating the content of key factors (e.g. MyD88, NF-κB) in the TLR-4/NF-κB pathway, contributing to its protective role against alcohol-induced liver injury. 3,5-DCQA also inhibited inflammation and apoptosis by recovering the key metabolites (e.g. phosphatidylserine) and related genes (e.g. Lpgat1) of glycerophospholipid metabolism. These results were further verified by transcriptomic and metabolomic analyses, showing that 3,5-DCQA exerts protective effects against alcohol-induced liver injury by modulating glycerophospholipid metabolism and suppressing oxidative stress, inflammation, and apoptosis through the TLR-4/NF-κB pathway. The current findings highlight the hepatoprotectivity of 3,5-DCQA and may facilitate the application of Gongju chrysanthemum in liver-protective functional foods.
研究领域:
肝脏病学
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分子生物学
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药理学
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营养科学
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代谢组学
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转录组学
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天然产物化学
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氧化应激
✓ 已验证
产品关联
DOI
PubMed
高影响因子
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
·
2018
·
IF 2.559
Fan Zhang,Chenhong Zhang
Intracerebral hemorrhage (ICH) is reported as a common and often fatal type of stroke accompanied with high morbidity and mortality, and it frequently results in long-lasting neurological dysfunctions. However, the pathogenesis that contributes to ICH has not been fully understood. Rnf112, also known as Znf179, is a member of the RING finger protein family. The expression of Rnf112 is abundant in the brain and is modulated during brain progression and development. The study aimed to explore the role of Rnf112 in brain injury after ICH, as well as the underlying molecular mechanisms. The results indicated that ICH led to a significant decrease in Rnf112, which was confirmed in oxyhemoglobin (oxyHb)-incubated astrocytes and microglial cells. Moreover, the Rnf112 knockout (Rnf112 −/− ) mice and wild type (WT) mice induced by ICH were further employed. Compared to the WT/ICH group, Rnf112 −/− mice exhibited accelerated brain injury, as evidenced by the increased brain water contents and neurological deficit scores (NDS). In comparison to WT/ICH group, a remarkable up-regulation in the release of pro-inflammatory cytokines, including tumor necrotic factor-α (TNF-α), interleukin-6 (IL-6), and IL-1β, was observed in perihematoma tissues of Rnf112 −/− mice on day 3 post-ICH. The process was along with promoted glial fibrillary acidic protein (GFAP) and Iba1 expression and reduced NeuN levels. Furthermore, ICH-induced increases in toll-like receptor (TLR)-4 and myeloid differentiation primary response protein (MyD88) expression were exacerbated by the loss of Rnf112. The phosphorylated expression of IKKα, inhibitor of NF-κB (IκBα) and nuclear factor-kappa B (NF-κB) induced by ICH in perihematoma tissues of mice was markedly enhanced in Rnf112 −/− mice. Rnf112 repression-induced inflammatory response was verified in lipopolysaccharide (LPS)-incubated glial cells . In contrast, over-expressing Rnf112 markedly attenuated ICH-induced brain injury by restraining inflammation via inactivating TLR-4/NF-κB pathway. In summary, our findings suggested that Rnf112 expression was highly involved in the progression of ICH, and targeting Rnf112 signaling might be a promising therapeutic strategy against ICH development.
研究领域:
神经科学
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分子生物学
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病理学
✓ 已验证
DOI
PubMed
高影响因子
危险品化学品经营许可证（带存储）