Annals of Dermatology
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2024
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IF 1.5
Lin-Xia Liu,Zhi-Kai Liao,Bing-Qi Dong,Shan Jiang,Tie-Chi Lei
Background Although reports suggest that tranexamic acid (TXA) has clinical benefits for melasma patients by oral, intralesional and topical treatment, the optimal route of TXA therapy and the underlying mechanism involved remain poorly defined. Objective To compare the skin lightening effect between oral TXA and topical TXA and to dissect the molecular mechanisms using ultraviolet B (UVB)-induced hyperpigmentation mouse model, ex vivo cultured human skin explant, and cultured melanocytes (MCs) and endothelial cells. Methods Melanin content and cluster of differentiation 31 (CD31)-positive cell numbers were measured in tail skins from UVB-irradiated mice treated by intragastral or topical TXA using immunofluorescent and Fontana-Masson staining. The conditioned medium (CM) was harvested from human umbilical vein endothelial cells treated with or without 3 mM TXA and was used to treat MCs for 48 hours. mRNA and protein levels of tyrosinase and microphthalmia-associated transcription factor were measured using quantitative real-time reverse transcription polymerase chain reaction and western blotting assays. HMB45- and CD31-positive cell numbers as well as melanin content were also examined in ex vivo cultured human skin explants. Results The hyperpigmented phenotype were significantly mitigated in UVB-irradiated tail skin plus intragastral TXA-treated mice compared with mice treated with UVB only or with UVB plus topical TXA. CD31-positive cell numbers correlated with the anti-melanogenic activity of TXA therapy. The data from cultured cells and skin tissues showed that suppression of endothelin-1 (ET-1) in vascular endothelial cells by TXA reduced melanogenesis and MC proliferation. Conclusion Oral TXA outperforms topical TXA treatment in skin lightening, which contributes to suppression of ET-1 in dermal microvascular endothelial cells by TXA.
研究领域:
皮肤病学
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分子生物学
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药理学
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DOI
PubMed
高影响因子
Cell Communication and Signaling
·
2023
·Vol. 21
·期 1
·1-17
·
IF 8.4
Zhao Weiming,Wang Lan,Yang Juntang,Chen Xinyu,Guo Xiaoshu,Xu Kai,Wang Ningdan,Zhao Wenyu,Xia Cong,Lian Hui,Rosas Ivan,Yu Guoying
Background Matrix metalloproteinases (MMPs) play important roles in remodeling the extracellular matrix and in the pathogenesis of idiopathic pulmonary fibrosis (IPF). MMP19, which is an MMP, was significantly upregulated in hyperplastic alveolar epithelial cells in IPF lung tissues and promoted epithelial-mesenchymal transition (EMT). Recent studies have demonstrated that endothelial-to-mesenchymal transition (E(nd)MT) contributes to pulmonary fibrosis. However, the role of MMP19 in pulmonary vascular injury and repair and E(nd)MT remains unclear. Methods To determine the role of MMP19 in E(nd)MT and pulmonary fibrosis. MMP19 expressions were determined in the lung endothelial cells of IPF patients and bleomycin (BLM)-induced mice. The roles of MMP19 in E(nd)MT and endothelial barrier permeability were studied in the MMP19 cDNA-transfected primary human pulmonary microvascular endothelial cells (HPMECs) and MMP19 adenoassociated virus (MMP19-AAV)-infected mice. The regulatory mechanism of MMP19 in pulmonary fibrosis was elucidated by blocking its interacting proteins SDF1 and ET1 with AMD3100 and Bosentan, respectively. Results In this study, we found that MMP19 expression was significantly increased in the lung endothelial cells of IPF patients and BLM-induced mice compared to the control groups. MMP19 promoted E(nd)MT and the migration and permeability of HPMECs in vitro, stimulated monocyte infiltration into the alveolus, and aggravated BLM-induced pulmonary fibrosis in vivo. SDF1 and Endothelin-1 (ET1) were physically associated with MMP19 in HPMECs and colocalized with MMP19 in endothelial cells in IPF patient lung tissues. AMD3100 and bosentan alleviated the fibrosis induced by MMP19 in the BLM mouse model. Conclusion MMP19 promoted E(nd)MT by interacting with ET1 and stimulated monocyte infiltration into lung tissues via the SDF1/CXCR4 axis, thus aggravating BLM-induced pulmonary fibrosis. Vascular integrity regulated by MMP19 could be a promising therapeutic target for suppressing pulmonary fibrosis.
Video abstract
研究领域:
呼吸病学
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细胞生物学
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分子生物学
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病理学
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DOI
PubMed
高影响因子
ENVIRONMENTAL TOXICOLOGY
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2023
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IF 4.5
Yujing Wang,Min Xiao,Feng Cai,Yang Li,Tianli Shi,Xiaoyan Zhou,Shuhong Tian,Denggao Huang
Vascular calcification (VC) is a common complication of chronic kidney disease (CKD). VC is a gene-regulated process similar to osteogenic differentiation. There are still no convincing schemes to prevent and reduce the development of VC. It has been reported that hypoxia-inducing factor 1α (HIF-1α) and endothelin-1(ET-1) are related to VC. In this study, we found that the expression of ET-1 and HIF-1α was enhanced after VC, the interaction between HIF-1α and ET-1 was confirmed by CO-IP and luciferase experiments. We found that ET-1 was an upregulated differential gene of calcified vascular smooth muscle cells (VSMCs) through gene sequencing. However, hypoxia-inducing factor 2α (HIF-2α) and HIF-1α have antagonistic effects on each other. HIF-1α is a pro-inflammatory cytokine, and HIF-2α can improve inflammation and fibrosis. Roxadustat, as a selective PHD3 inhibitor, preferentially activates HIF-2α. It is still unclear whether roxadustat improves VC in CKD by regulating the expression of HIF-2α/HIF-1α. Alizarin red staining and western blot as well as immunohistochemical results showed that roxadustat could significantly reduce the degree of vascular and VSMCs calcification in CKD rats. Serum HIF-1α and ET-1 were significantly decreased after roxadustat treatment. In addition, western blot results showed that roxadustat could decrease the expression of HIF-1α and ET-1 in vascular tissues and calcified VSMC, but HIF-2α expression significantly increased. Interestingly, our study confirmed that activation of HIF-1α or inhibition of HIF-2α reversed the ameliorating effect of roxadustat on VC, proving that the effect mediated by roxadustat is HIF-2α/HIF-1α dependent. We have demonstrated for the first time that roxadustat improves VC in CKD rats by regulating HIF-2α/HIF-1α, thus providing a new idea for the application of roxadustat in VC of CKD.
研究领域:
药理学
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肾病学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
Cells
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2021
·Vol. 10
·期 6
·1359
·
IF 6.6
Nashwa Amin,Shijia Chen,Qiannan Ren,Xiaoning Tan,Benson O. A. Botchway,Zhiying Hu,Fengpei Chen,Shan Ye,Xiaoxue Du,Zuobing Chen,Marong Fang
Hypoxia-inducible factor 1 can sufficiently control the progress of neurological symptoms after ischemic stroke owing to their actions associated with its downstream genes. In this study, we evaluated the role of HIF-1α in attenuating brain damage after endothelin-1 injection. Focal cerebral ischemia in mice were induced by endothelin-1 microinjection. Hypoxia-inducible factor 1 activator, dimethyloxalylglycine (DMOG), and HIF-1α inhibitor, acriflavine (ACF), were used to evaluate the hypoxia-inducible factor 1 activity during cerebral ischemia. The expression levels of HIF-1α, glial fibrillary acidic protein (GFAP), interleukin-10 (IL-10), inducible nitric oxide synthase (iNOS), phosphorylated I-kappa-B-alpha/total I-kappa-B-alpha (p-IκBα/IκBα) and nuclear factor kappa B (NF-kB) were assessed. Besides, mRNA levels of IL-10, tumor necrosis factor- alpha (TNF-α), and NF-kB were also analyzed. Results showed a noticeable increase in hypoxia-inducible factor 1 and IL-10 levels in the DMOG group with a decline in iNOS, TNF-α, and NF-kB levels, implying the anti-inflammatory role of hypoxia-inducible factor 1 activator following stroke. These findings were further corroborated by GFAP immunostaining that showed astrocytic activation to be inhibited 12 days post-ischemia, as well as histological and TEM analyses that demonstrated hypoxia-inducible factor 1 induction to alleviate neuronal soma damage and cell death. Based on our study, HIF-1α could be a potential therapeutic target for ischemic stroke.Keywords:endothelin-1;hypoxia-inducible factor-1;interleukin 10;astrocyte;dimethyloxalylglycine;acriflavine;proinflammatory cytokines
研究领域:
神经科学
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药理学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
Food Bioscience
·
2025
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IF 5.9
Wenyun Xiong,Yan Zhang,Lixia Guo,Shuai Zhao,Di Zhang,Zihuan Wu,Shengbao Cai
The novel peptide LADW has umami taste characteristic, while its health benefits and gastrointestinal stability have not been investigated. This study used in vitro and in silico experiments to investigate the effects and mechanisms of this peptide on angiotensin I-converting enzyme (ACE1) and vascular function, and its gastrointestinal stability was also evaluated by a simulated digestion. Results demonstrated that LADW exhibited a good inhibitory effect against ACE1, with an IC 50 value of 28.02 ± 1.52 μM. Kinetics, isothermal titration calorimetry, and thermal shift assay revealed that LADW competitively binds ACE1, with multi-site, entropy-driven interactions and slight conformational modulation. Molecular docking and molecular dynamics simulations showed that the LADW effectively bound to the active site of ACE1 mainly through hydrogen bonding and hydrophobic interactions, stabilized the conformation of ACE1, and reduced the fluctuation of the most active amino acid residues, such as Glu411, Ala354 and Glu384. Meanwhile, the LADW promoted the nitric oxide (NO) release and inhibited the endothelin-1 (ET-1) secretion. Further analysis showed that the LADW formed strong interactions with several key proteins in the regulation of NO and ET-1 release, namely endothelial nitric oxide synthase, endothelin-converting enzyme-1 and Furin. In addition, the LADW showed a good gastrointestinal stability after a simulated gastrointestinal digestion in vitro with a retention rate of 48.37 ± 3.00 %. The findings of this study may contribute to the elucidation of the potential benefits of the peptide LADW in reducing blood pressure and safeguarding the cardiovascular system, thereby offering a foundation for further research.
研究领域:
生物化学
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药理学
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心血管研究
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计算生物学
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营养科学
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产品关联
DOI
高影响因子
Food Bioscience
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2024
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IF 4.8
Zishan Dou,Yang Xu,Jingli Liu,Wei Chen
LVLPGE is an angiotensin-converting enzyme (ACE) inhibitory peptide extracted from broccoli protein hydrolysates. The antihypertensive mechanism of LVLPGE was explored in the present study. The results indicated that the IC 50 value of LVLPGE was 19.49 μM, and its binding to ACE occurred via a static fluorescence quenching involving the secondary structure changes of ACE. In addition, LVLPGE competitively bound to the active site of ACE through hydrogen bonding. Furthermore, LVLPGE markedly enhanced the levels of the vasodilator nitric oxide (NO) in the Ang I-induced HUVECs model, suppressed the expression of vasoconstrictor endothelin-1 (ET-1), and increased the phosphorylation of eNOS. Moreover, LVLPGE was found to enhance the production of cyclic guanosine monophosphate (cGMP), which leading to a subsequent decrease in intracellular calcium concentration, ultimately facilitating the relaxation of vascular smooth muscles and lowering the blood pressure. These results demonstrated that LVLPGE achieves the antihypertensive effects by inhibiting ACE activity and activating the eNOS/NO/cGMP signaling pathway. This study provides new insights into the antihypertensive mechanism of LVLPGE and contributes to the high-value utilization of broccoli resources.
研究领域:
药理学
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心血管科学
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功能性食品
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生物化学
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产品关联
DOI
高影响因子
JOURNAL OF CELLULAR PHYSIOLOGY
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2018
·Vol. 234
·期 3
·2537-2551
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IF 3.923
Hai-Ming Xu,Feng-Hua Sui,Mei-Hua Sun,Gong-Liang Guo
Recent studies have shown that circulating microRNAs (miRNA) play a critical role in diagnosing acute coronary syndrome (ACS). This study aims to investigate the effect of miR-224 on atherosclerotic plaques forming and vascular remodeling in ACS and its relationship with TGF-β/Smad pathway. Myocardial infarction (MI) rat model was established and lentivirus vector of miR-224 inhibitor was prepared for investigating the effect of downregulated miR-224 on the contents of nitric oxide (NO) and endothelin-1 (ET-1), blood lipid levels and inflammatory factor levels in serum as well as the TGF-β/Smad pathway. The rats suffering from MI had decreased survival rates and exhibited reduced levels of NO, high-density lipoprotein cholesterol, and lumen diameter, and Smad7 messenger RNA (mRNA) and protein expression; while had significantly increased ratio of heart weight or body weight, levels of ET-1, inflammatory factors, blood lipid indexes, vascular remodeling indexes, collagen volume fraction, vulnerable atherosclerotic plaque area, VCAM-1 and MMP-2 protein expression, TGF-β, Smad2, Smad3, and Smad4 mRNA and protein expression. After inhibiting the TGF-β/Smad pathway, the rats suffering from MI showed notably opposite trend. In conclusion, downregulation of miR-224 expression promotes the formation of vulnerable atherosclerotic plaques and vascular remodeling in ACS through activation of the TGF-β/Smad pathway. Therefore, this study provides a new therapeutic target for ACS.
研究领域:
心脏病学
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分子生物学
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病理生理学
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产品关联
DOI
PubMed
高影响因子
Food Science and Human Wellness
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2022
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IF 8.022
Xiaofeng Zhang,Zhenhua Liang,Geoffrey Ivan Neil Waterhouse,Shengjun Jiang,Dongxiao Sun-Waterhouse,Jinmei Wang,Changyang Ma,Wenyi Kang
This is the first report on a polysaccharide (RCJ2-Ib) isolated from Rosa Chinensis Flos. RCJ2-Ib was obtained through the extraction with water, precipitation with ethanol, separation with DEAE-52 column and purification with DEAE-Sepharose Fast Flow column and Sephadex G100 column. GC, FT-IR and NMR analyses revealed that RCJ2-Ib (3.3 kDa) was a 1,4-linked polymannuronic acid containing substantial β - D -anomers units. The anticoagulant effect of RCJ2-Ib evaluated by using rabbit ear venous blood and an acute blood stasis rat model showed that RCJ2-Ib had obvious anticoagulant activity in regulating endogenous and exogenous coagulation pathways and reducing serum thromboxane B2 and endothelin-1. In addition, RCJ2-Ib could also increase the number of Lactobacillus and Escherichia coli . As a result, RCJ2-Ib has the potential to inhibit thrombosis and maintain the intestinal environment.
研究领域:
药理学
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生物化学
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医学
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产品关联
DOI
高影响因子
PHYTOMEDICINE
·
2019
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IF 4.18
Ziru Zhang,Jianbo Ji,Dawei Zhang,Maoqiang Ma,Longru Sun
Background The root of Salvia miltiorrhiza f. alba (RSMA) (Lamiaceae) is used for the treatment of patients with thromboangiitis obliterans (TAO) in traditional Chinese medicine . Previously, a mixture of phenolic acids extracted from RSMA has shown significant protective effects on TAO rats. Purpose This study investigates the inhibitory effects of salvianolic acid B on TAO induced by sodium laurate injection in rats to explore the effective constituents of RSMA in TAO treatment. Methods TAO rats were developed using injected sodium laurate. After treatment with ligustrazine hydrochloride (15 mg/kg) and various doses of salvianolic acid B (10, 20, 40 mg/kg) by tail intravenous injection , levels of thromboxane B 2 (TXB 2 ), 6-keto-prostaglandin F 1α (6-keto-PGF 1α ) and endothelin-1 (ET-1) in plasma were determined using enzyme-linked immunosorbent assay. The right femoral arteries were studied by hematoxylin and eosin staining and immunohistochemical analysis to determine pathological changes and overexpression of tumor necrosis factor (TNF)–α and inducible nitric oxide synthase (iNOS) in the femoral artery walls of TAO rats. Results Salvianolic acid B significantly decreased the expressions of TXB 2 and ET-1 and increased the expression of 6-keto-PGF 1α in plasma, and significantly inhibited the overexpression of TNF-α and iNOS in the femoral artery walls of TAO rats at medium and high doses. Conclusion Salvianolic acid B has a protective effect on TAO rats. The mechanism may involve inhibition of thrombosis and TAO-associated inflammatory responses, which may explain the success of RSMA treatment of TAO in humans in traditional Chinese medical practice. Hence, it may be a potential drug for TAO treatment in conventional medicine.
研究领域:
药理学
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免疫学
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病理学
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传统中药
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心血管疾病
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产品关联
DOI
PubMed
高影响因子
Chinese Medicine
·
2021
·Vol. 16
·期 1
·1-21
·
IF 5.455
Li Qiaofeng,Lan Taijin,He Songhua,Chen Weiwei,Li Xiaolan,Zhang Weiquan,Liu Ying,Zhang Qiuping,Chen Xin,Han Yaoyao,Su Zhiheng,Zhu Dan,Guo Hongwei
Background Lei-gong-gen formula granule (LFG) is a folk prescription derived from Zhuang nationality, the largest ethnic minority among 56 nationalities in China. It consists of three herbs, namely Eclipta prostrata (L.) L., Smilax glabra Roxb, and Centella asiatica (L.) Urb. It has been widely used as health protection tea for hundreds of years to prevent hypertension in Guangxi Zhuang Autonomous Region. The purpose of this study is to validate the antihypertensive effect of LFG on the spontaneously hypertensive rat (SHR) model, and to further identify the effective components and anti-hypertension mechanism of LFG.Methods The effects of LFG on blood pressure, body weight, and heart rate were investigated in vivo using the SHR model. The levels of NO, ANG II, and ET-1 in the serum were measured, and pathological changes in the heart were examined by H&E staining. The main active components of LFG, their corresponding targets, and hypertension associated pathways were discerned through network pharmacology analysis based on the Traditional Chinese Medicine Systems Pharmacology (TCMSP), Traditional Chinese Medicine Integrated Database (TCMID), and the Bioinformatics Analysis Tool for Molecular Mechanism of Traditional Chinese Medicine (BATMAN-TCM). Then the predicted results were further verified by molecular biology experiments such as RT-qPCR and western blot. Additionally, the potential active compounds were predicted by molecular docking technology, and the chemical constituents of LFG were analyzed and identified by UPLC-QTOF/MS technology. Finally, an in vitro assay was performed to investigate the protective effects of potential active compounds against hydrogen peroxide (H2O2) induced oxidative damage in human umbilical vein endothelial cells (HUVEC).Results LFG could effectively reduce blood pressure and increase serum NO content in SHR model. Histological results showed that LFG could ameliorate pathological changes such as cardiac hypertrophy and interstitial inflammation. From network pharmacology analysis, 53 candidate active compounds of LFG were collected, which linked to 765 potential targets, and 828 hypertension associated targets were retrieved, from which 12 overlapped targets both related to candidate active compounds from LFG and hypertension were screened and used as the potential targets of LFG on antihypertensive effect. The molecular biology experiments of the 12 overlapped targets showed that LFG could upregulate the mRNA and protein expressions of NOS3 and proto-oncogene tyrosine-protein kinase SRC (SRC) in the thoracic aorta. Pathway enrichment analysis showed that the PI3K-AKT signaling pathway was closely related to the expression of NOS3 and SRC. Moreover, western blot results showed that LFG significantly increased the protein expression levels of PI3K and phosphorylated AKT in SHR model, suggesting that LFG may active the PI3K-AKT signaling pathway to decrease hypertension. Molecular docking study further supported that p-hydroxybenzoic acid, cedar acid, shikimic acid, salicylic acid, nicotinic acid, linalool, and histidine can be well binding with NOS3, SRC, PI3K, and AKT. UPLC-QTOF/MS analysis confirmed that p-hydroxybenzoic acid, shikimic acid, salicylic acid, and nicotinic acid existed in LFG. Pre-treatment of HUVEC with nicotinic acid could alleviate the effect on cell viability induced by H2O2 and increase the NO level in cell supernatants.Conclusion sLFG can reduce the blood pressure in SHR model, which might be attributed to increasing the NO level in serum for promoting vasodilation via upregulating SRC expression level and activating the PI3K-AKT-NOS3 signaling pathway. Nicotinic acid might be the potential compound for LFG antihypertensive effect.
研究领域:
药理学
·
分子生物学
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中药学
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心血管疾病
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产品关联
DOI
PubMed
高影响因子
CANCER SCIENCE
·
2022
·
IF 6.518
Jie Liu,Huxia Wang,Miao Zhang,Yazhao Li,Ruiqi Wang,He Chen,Bo Wang,Xiaoqian Gao,Shaoran Song,Yaochun Wang,Yu Ren,Juan Li,Peijun Liu
Multiple cancers have been reported to be associated with angiogenesis and are sensitive to anti‐angiogenic therapies. Vascular normalization, by restoring proper tumor perfusion and oxygenation, could limit tumor cell invasiveness and improve the effectiveness of anticancer treatments. However, the underlying anticancer mechanisms of antiangiogenic drugs are still unknown. Metformin (MET) and simvastatin (SVA), two metabolic‐related drugs, have been shown to play important roles in modulating the hypoxic tumor microenvironment and angiogenesis. Whether the combination of MET and SVA could exert a more effective antitumor effect than individual treatments has not been examined. The antitumor effect of the synergism of SVA and MET was detected in mouse models, breast cancer patient‐derived organoids, and multiple tumor cell lines compared with untreated, SVA, or MET alone. RNA sequencing revealed that the combination of MET and SVA (but not MET or SVA alone) inhibited the expression of endothelin 1 (ET‐1), an important regulator of angiogenesis and the hypoxia‐related pathway. We demonstrate that the MET and SVA combination showed synergistic effects on inhibiting tumor cell proliferation, promoting apoptosis, alleviating hypoxia, decreasing angiogenesis, and increasing vessel normalization compared with the use of a single agent alone. The MET and SVA combination suppressed ET‐1‐induced hypoxia‐inducible factor 1α expression by increasing prolyl hydroxylase 2 (PHD2) expression. Furthermore, the MET and SVA combination showed a more potent anticancer effect compared with bosentan. Together, our findings suggest the potential application of the MET and SVA combination in antitumor therapy.
研究领域:
肿瘤学
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药理学
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分子生物学
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癌症生物学
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产品关联
DOI
PubMed
高影响因子
Journal of Neuroimmune Pharmacology
·
2024
·Vol. 19
·期 1
·1-17
·
IF 5.2
Lin Yun,Liu Tian,Chen Hong,Zeng Ming,Hu Shunwei,Yu Xiaoning,Chen Yonghua,Xia Chunmei,Wang Jin,Wang Jijiang
The occurrence of major asthma symptoms is largely attributed to airway vagal hypertonia, of which the central mechanisms remain unclear. This study tests the hypotheses that endothelin-1-mediated brainstem glial activation produces asthmatic airway vagal hypertonia via enhanced action of adenosine 5’-triphosphate on neuronal purinergic P2X4 receptors. A rat model of asthma was prepared using ovalbumin. Airway vagal tone was evaluated by the recurrent laryngeal discharge and plethysmographic measurement of pulmonary function. The changes in the brainstem were examined using ELISA, Western blot, luciferin-luciferase, quantitative reverse transcription-polymerase chain reaction, enzyme activity assay and immunofluorescent staining, respectively. The results showed that in the medulla of rats, endothelin receptor type B and P2X4 receptors were primarily expressed in astrocytes and neurons, respectively, and both of which, along with endothelin-1 content, were significantly increased after ovalbumin sensitization. Ovalbumin sensitization significantly increased recurrent laryngeal discharge, which was blocked by acute intracisternal injection of P2X4 receptor antagonist 5-BDBD, knockdown of brainstem P2X4 receptors, and chronic intraperitoneal injection of endothelin receptor type B antagonist BQ788, respectively. Ovalbumin sensitization activated microglia and astrocytes and significantly decreased ecto-5’-nucleotidase activity in the medulla, and all of which, together with the increase of medullary P2X4 receptor expression and decrease of pulmonary function, were reversed by chronic BQ788 treatment. These results demonstrated that in rats, allergic airway challenge activates both microglia and astrocytes in the medulla via enhanced endothelin-1/endothelin receptor type B signaling, which subsequently causes airway vagal hypertonia via augmented adenosine 5’-triphosphate/P2X4 receptor signaling in central neurons of airway vagal reflex. Graphical Abstract
研究领域:
神经科学
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药理学
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呼吸医学
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免疫学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
危险品化学品经营许可证（带存储）