Literature Display

Article 1-3-B-RUT is a derivative of RUT that prevents alcohol induced liver damage by reducing inflammation and oxidative stress

Article Title：3-B-RUT, a derivative of RUT, protected against alcohol-induced liver injury by attenuating inflammation and oxidative stress

Published：International Immunopharmacology

Impact factor（IF）：4.932

DOI:https://doi.org/10.1016/j.intimp.2021.107471

Article topic：

Alcoholic liver disease (ALD) is the most common chronic liver disease worldwide. At present, there is no clear treatment for alcoholic liver injury (ALI). Inflammatory response and oxidative stress play crucial roles in ALI. Cyclooxygenase-2 (COX-2) can be induced by inflammation, and it has been reported that COX-2 expression is enhanced in alcoholic liver injury. Extract rutin (RUT) from Evodia rutaecarpa. RUT has a wide range of pharmacological activities. In order to enhance its anti-inflammatory activity, our group introduced sulfonyl groups to synthesize 3- [2- (trifluoromethoxy) benzenesulfonamide] - rutin (3-B-RUT). This study investigated the protective effect of 3-B-RUT on alcoholic liver injury in vitro and in vivo, and preliminarily explored its mechanism of action. Establish a mouse ALI model based on the chronic ethanol drinking model. The results showed that 3-B-RUT (20 μ g/kg) can alleviate alcoholic liver injury, inhibit liver inflammation and oxidative stress, and the effect is comparable to RUT (20 mg/kg). The in vitro results are consistent with the in vivo results. Mechanistically, 3-B-RUT may inhibit inflammatory responses and oxidative stress by regulating the activation of the NF - κ B/COX-2 pathway. In summary, the derivative 3-B-RUT of RUT may be a promising clinical candidate for ALI treatment. Mechanistically, 3-B-RUT may inhibit inflammatory responses and oxidative stress by regulating the activation of the NF - κ B/COX-2 pathway. In summary, the derivative 3-B-RUT of RUT may be a promising clinical candidate for ALI treatment. Mechanistically, 3-B-RUT may inhibit inflammatory responses and oxidative stress by regulating the activation of the NF - κ B/COX-2 pathway. In summary, the derivative 3-B-RUT of RUT may be a promising clinical candidate for ALI treatment.

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Article 2- Upregulation of Thrombopoietin Expression through ROS Dependent Src/ERK/STAT3 Signaling Pathway for the Treatment of Thrombocytopenia

Title of the article：Photobiomodulation Therapy for Thrombocytopenia by Upregulating Thrombopoietin Expression via the ROS-dependent Src/ERK/STAT3 Signaling Pathway

Published：J Thromb Haemost

Impact factor（IF）：4.157

DOI:10.1111/JTH.15252

Article topic:

Chemotherapy induced thrombocytopenia (CIT) increases the risk of bleeding, which may delay or prevent the implementation of anti-cancer treatment plans. Photobiomodulation therapy (PBMT) is a non-invasive physical therapy proposed to improve thrombocytopenia; However, its potential regulatory mechanisms are not fully understood.

Further explore the mechanism of action of thrombopoietin (TPO) in megakaryocyte and platelet production.

We used various methods such as western blotting, cell transfection, flow cytometry, and animal experiments to explore the effects and mechanisms of PBMT on platelet production. PBMT prevented a severe decrease in platelet count by increasing platelet production, and then improved CIT. Mechanistically, PBMT significantly upregulates liver TPO expression in a mouse model of thrombocytopenia, thereby promoting megakaryocyte and platelet production. PBMT increases the levels of TPO mRNA and protein through the Src/ERK/STAT3 signaling pathway in liver cells. In addition, the generation of reactive oxygen species is the reason for PBMT induced Src activation and its downstream target effects. Our research suggests that PBMT is a promising treatment strategy for CIT.

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Article 3- Endoplasmic reticulum stress induced by reactive oxygen species mediates epithelial mesenchymal transition and pulmonary fibrosis induced by 1-nitropyrene

Title of the article：Reactive oxygen species-evoked endoplasmic reticulum stress mediates 1-nitropyrene-induced epithelial-mesenchymal transition and pulmonary fibrosis

Published Journal：Environmental Pollution

Impact factor（IF）：6.792

DOI:https://doi.org/10.1016/j.envpol.2021.117134

Article topic：

1-nitropyrene (1-NP) is a component of atmospheric fine particles. Previous reports have shown that acute exposure to 1-NP can cause respiratory inflammation. The aim of this study is to investigate whether chronic exposure to 1-NP can induce pulmonary fibrosis. Infuse 1-NP (20 μ g/mouse/week) into the trachea of male C57BL6/J mice for 6 weeks. Diffuse interstitial inflammation, a-smooth muscle actin (a-SMA) positive cells, markers of epithelial mesenchymal transition (EMT), and extensive collagen deposition were observed in the lungs of mice exposed to 1-NP, as measured by Masson staining Pulmonary function showed a decrease in lung dynamic compliance (Cydn min) in mice exposed to 1-NP. On the contrary, the inspiratory resistance (Ri) and expiratory resistance (Re) of mice exposed to 1-NP increased. Mechanistically, cell migration and invasion are accelerated in lung epithelial cells exposed to 1-NP. In addition, the epithelial marker E-cadherin is downregulated, while the three mesenchymal markers of vimentin, a-SMA, and N-cadherin are upregulated in lung epithelial cells exposed to 1-NP. Although TGF - β did not change, phosphorylated Smad2/3 was enhanced in lung epithelial cells exposed to 1-NP. In addition, in lung epithelial cells exposed to 1-NP, reactive oxygen species (ROS) increased and endoplasmic reticulum (ER) stress was activated. N-acetylcysteine (NAC) is an antioxidant that can reduce excessive ROS, ER stress, and EMT induced by 1-NP in lung epithelial cells. Similarly, pretreatment with NAC can alleviate pulmonary EMT and pulmonary fibrosis induced by 1-NP in mice.

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