ACS Sensors
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2022
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IF 9.618
Zhidong Qiu,Chaobang Zhang,Liangliang Zhang,Shulong Wang,Shengqiang Hu,Shulin Zhao
The interaction between light and biological tissues in the second near-infrared (NIR-II) window is weak, which can effectively reduce the scattering and absorption of incoming light by biological tissues and enhance the resolution and sensing ability of in vivo photoacoustic (PA) imaging. In particular, tissues that carry blood and water produce the lowest PA background in the wavelength range of 1050 to 1150 nm. However, the development of the NIR-II PA probe for the above window faces great challenges. To tackle this challenge, the reduction–reoxidation of an organic dye was used to develop a PA imaging probe (Hydro-1048) as the first NIR-II PA probe of a hydroxy radical (·OH) for molecular imaging in deep tissue. The ·OH oxidized the C–N single bond in Hydro-1048 to double bonds, which formed Et-1065. This conversion extended the conjugate system of the molecule and shifted the absorption peak from 520 to 1065 nm, which resulted in a strong PA signal after irradiation with a 1065 nm laser. At a detection limit of 0.6 nM, a good linear relationship within the range of 5–1000 nM was obtained for the PA signal intensity versus the concentration of ·OH. The developed NIR-II PA probe can be used for the noninvasive high-resolution imaging of ·OH in deep tissue, and the PA imaging of ·OH can also be used to visually monitor in situ pathological processes related to hepatitis.
研究领域:
生物医学工程
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分子影像学
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病理学
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DOI
PubMed
高影响因子
ENVIRONMENTAL POLLUTION
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2025
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IF 7.3
Zixu Li,Yacan Gong,Emmanuel Sunday Okeke,Dan Li,Yao Chen,Weiwei Feng,Ting Zhao,Liuqing Yang,Guanghua Mao,Xiangyang Wu
Typical plasticizer dibutyl phthalate (DBP) has been demonstrated to induce hepatotoxicity in zebrafish, but the underlying molecular mechanisms remain incompletely elucidated. Numerous studies have shown that ferroptosis is involved in the pathophysiological progression of hepatic disease. However, it remains unclear whether ferroptosis is involved in the DBP-induced hepatotoxicity in zebrafish. Initially, histopathological analyses have preliminarily confirmed that DBP can activate inflammatory responses in the zebrafish liver. Further investigation revealed that DBP induces ferroptosis in the zebrafish liver, characterized by iron overload, lipid peroxidation, and aberrant activation of ferroptosis pathways. Furthermore, DBP exposure induced ferroptosis, disrupting cell membranes and subsequent release of HMGB1, which are sensed by immunocytes TLR4/NF-κB signaling pathways, thereby activating the innate immune response in a context-dependent manner. Moreover, the ferroptosis inhibitor Fer-1 effectively rescues the activation of HMGB1-TLR4/NF-κB-mediated immune processes. Overall, this work enriches the molecular mechanism of DBP-induced zebrafish liver inflammatory damage and provides a reliable biomarker for future environmental risk assessment of DBP.
研究领域:
环境毒理学
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分子生物学
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免疫学
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产品关联
DOI
PubMed
高影响因子
POULTRY SCIENCE
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2025
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IF 4.2
Qiyue Zhang,Yue Wang,Yanwei Wang,Jielu Yuan,Yaru Wang,Yongqi Zeng,Haihua Zhang,Hui Yang,Qiugang Ma,Donghui Shi,Shimeng Huang
This study investigates the effects of 3-indoleacrylic acid (IAA), a bacterial metabolite of tryptophan, on LPS-induced liver injury in laying hens. The aim is to explore the potential hepatoprotective mechanisms of IAA, particularly through the modulation of inflammatory and antioxidant pathways. A total of 48, 24-week-old No. 6 Jingfen laying hens were randomly divided into four groups of 12 hens each: the CON group (basal diet), IAA group (basal diet + 150 mg/kg IAA), LPS group (basal diet), and IAA+LPS group (basal diet + 150 mg/kg IAA). The feeding period lasted 8 weeks, and at the end of the 8th week, the laying hens in the LPS and IAA+LPS groups were intraperitoneally injected with 0.5 mg/kg LPS. The four groups were uniformly slaughtered and sampled 12 hours after LPS injection. The expression of pro-inflammatory cytokines (IL-1β, TNF-α, IL-6) was significantly alleviated ( P < 0.05), and antioxidant enzymes (T-SOD, CAT, GSH-PX) were significantly elevated ( P < 0.05) in the serum and liver of the IAA+LPS group. Histological analysis revealed reduced hepatocyte necrosis and inflammation in the IAA-treated groups ( P < 0.05). Additionally, the activation of MAPK and Toll-like receptor (TLR) signaling pathways was modulated through transcript analyses, thereby reducing inflammation and oxidative stress. In summary, IAA effectively mitigates liver inflammation and oxidative stress through the regulation of MAPK and TLR signaling pathways, providing a promising strategy for improving liver health in hens. This study represents the first report on the application of IAA in poultry, demonstrating its potential as a novel therapeutic agent for alleviating liver injury.
研究领域:
动物科学
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免疫学
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分子生物学
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DOI
PubMed
高影响因子
FOOD AND CHEMICAL TOXICOLOGY
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2024
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IF 3.9
Yanan Wang,Qianqian Wang,Gaigai Wang,Qiongqiong Zhang,Yongpeng Guo,Xin Su,Yu Tang,Matthew Koci,Jianyun Zhang,Qiugang Ma,Lihong Zhao
Zearalenone (ZEN) poses a potential threat on human and animal health partly through the nuclear factor (NF)-κB signaling pathway. In silico study suggested that rutin effective against TLR4 and NF-κB. A wetting test was designed to evaluate the effect and underlying mechanism of rutin in alleviating ZEN-induced inflammation in animals. Twenty-four female mice were randomly divided into 4 groups: control (basal diet), ZEN group (basal diet + ZEN), rutin group (basic diet + rutin), Z + R group (basal diet + rutin + ZEN). Results showed that rutin effectively alleviated ZEN-induced inflammation and damage of liver and jejunum in mice. Rutin addition reduced the content of lipopolysaccharide (LPS) in serum and liver mainly by improving the intestinal barrier function resulted from the production increase of short-chain fatty acids (SCFA). In sum, this study showed that rutin alleviated ZEN-induced liver inflammation and injury by modulating the gut microbiota, increasing the production of SCFA and improving intestinal barrier function, leading to the decrease of LPS in liver and the inhibition of MyD88 independent NF-κB signaling pathway in mice. Specifically, these findings may provide useful insights into the screening of functional natural compounds and its action mechanism to alleviate ZEN induced liver inflammation.
研究领域:
药理学
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毒理学
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分子生物学
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免疫学
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DOI
PubMed
高影响因子
Cell Communication and Signaling
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2024
·Vol. 22
·期 1
·1-17
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IF 8.2
Zhang Yu,Wu Rong,Zhan Xi,Wang Xuan-Yi,Xiang Lin-Wei,Duan Ya-Qian,You Yan,Zhang Jian-Bo,Wu Rui,Zhang Yun-Yuan,Duan Liang
Background Absent in melanoma 2 (AIM2) inflammasome-dependent pyroptosis and neutrophil extracellular traps (NETs) have been implicated in chronic liver disease (CLD). However, the specific intrahepatic cell type that undergoes AIM2 inflammasome-dependent pyroptosis and how their interaction augments hepatic inflammation/fibrosis remains unclear.Methods The expression and correlation of AIM2 inflammasome-dependent pyroptosis-related indicators and NETs were analyzed in biopsy tissue and blood specimens from chronic hepatitis patients (CHs). Cell-based experiments were conducted to investigate their interaction. In vitro and in vivo experiments were used to analyze their effects on the progression of hepatic inflammation/fibrosis as well as their clinical importance.Results Elevated levels of AIM2 inflammasome-dependent pyroptosis indicators and NETs were detected in biopsy tissue and blood specimens. Circulating NETs were positively correlated with pyroptosis-related indicators, and both were related with disease severity. Confocal imaging revealed that AIM2 was mainly localized to hepatic macrophages, indicating that hepatic macrophages were the major cell type that underwent pyroptosis. NETs were directly engulfed by macrophages and then stimulated AIM2 inflammasome-dependent macrophage pyroptosis in vitro, which amplified the activation of hepatic stellate cells (HSCs) and increased collagen deposition. Administration of the NETs degradation agent DNase I or the AIM2 inflammasome activation inhibitor ODN A151 effectively alleviated chronic liver inflammation/fibrosis progression in vivo.Conclusion sNETs-induced AIM2 inflammasome-dependent pyroptosis in macrophages facilitates liver inflammation/fibrosis progression. The identified NET–AIM2 inflammasome cascade could serve as a novel therapeutic target for hepatic inflammation/fibrosis progression.
研究领域:
免疫学
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肝病学
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细胞生物学
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分子生物学
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DOI
PubMed
高影响因子
危险品化学品经营许可证（带存储）