PMC:7396557 / 33353-36403 JSON TXT

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LitCovid-PMC-OGER-BB

LitCovid-PD-FMA-UBERON

LitCovid-PD-UBERON

LitCovid-PD-MONDO

LitCovid-PD-CLO

LitCovid-PD-CHEBI

LitCovid-PD-GO-BP

{"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T46","span":{"begin":1231,"end":1260},"obj":"http://purl.obolibrary.org/obo/GO_0050776"},{"id":"T47","span":{"begin":1245,"end":1260},"obj":"http://purl.obolibrary.org/obo/GO_0006955"},{"id":"T48","span":{"begin":1264,"end":1279},"obj":"http://purl.obolibrary.org/obo/GO_0016032"},{"id":"T49","span":{"begin":1555,"end":1564},"obj":"http://purl.obolibrary.org/obo/GO_0046903"},{"id":"T50","span":{"begin":2437,"end":2458},"obj":"http://purl.obolibrary.org/obo/GO_0006954"},{"id":"T51","span":{"begin":2528,"end":2545},"obj":"http://purl.obolibrary.org/obo/GO_0007165"},{"id":"T52","span":{"begin":2528,"end":2537},"obj":"http://purl.obolibrary.org/obo/GO_0023052"}],"text":"Progress of Pharmacological Research on LHQWC\nModern pharmacological studies have shown that LHQWC has antiviral, immune-regulatory, anti-inflammatory, and antioxidant properties, efficacy against lung injury, and other effects (see Table 3 ).\nLHQWC significantly inhibited SARS-CoV-2 replication in Vero E6 cells and markedly reduced the production of pro-inflammatory cytokines (TNF-α, IL-6, CCL-2/MCP-1, and CXCL-10/IP-10) at the mRNA level. Furthermore, LHQWC treatment resulted in abnormal virion particle morphology in cells. LHQWC significantly inhibits SARS-CoV-2 replication, affects virus morphology and exerts anti-inflammatory activity in vitro (Li R. F. et al., 2020).\nIn vitro experiments have shown significant antiviral activity against SARS-CoV, AIV H7N9, dual H1N1/H3N2, together with inhibition of Middle East Respiratory Syndrome (MERS)-CoV activity to a certain degree (Yao et al., 2020). Yuewen Ding et al. used MTT and plaque reduction assays to show that LHQWC inhibited proliferation of multiple strains of influenza virus, and reduced virus titer and levels of inflammatory cytokines in the lungs of infected mice. The results indicated that LHQWC acted as a broad-spectrum antiviral and, in particular, regulated the immune response to viral infection (Ding et al., 2017). Qi Li et al. discovered that LHQWC not only reversed LPS-stimulated expression of macrophage chemotactic factor-1 (MCP-1) by macrophages, but also significantly improved pulmonary edema in a mouse model of acute lung injury. Inhibition of expression and secretion of MCP-1 in lung tissues of model mice was accompanied by reduced infiltration of mononuclear macrophages and reduction of inflammatory injury (Li et al., 2019). Fen Ping et al. studied the effects of LHQWC on rats with oxidative lung injury caused by fine particulate matters (PM 2.5). The results showed that LHQWC significantly reduced lactate dehydrogenase (LDH) and malondialdehyde (MDA) serum levels in rats with lung injury, increased levels of glutathione peroxidase (GSH-Px), reduced pathological damage of lung tissues, and inhibited exudation of inflammatory cells into the alveolar cavity. Together, the data indicated that LHQWC protected against oxidative stress injury in the lungs of rats (Ping et al., 2016). Wenwen Cui et al. studied the impact of LHQWC in a mouse model of acute lung injury caused by intratracheal infusion of LPS. LHQWC alleviated the inflammatory response in lung tissues by downregulating the IKK/IκB/nuclear factor (NF)-κB signaling pathway, thus, protecting mice from acute lung injury (Cui et al., 2016). Siwen Tang et al. studied the effects of LHQWC intervention on pathological lung tissue injury in mice and expression of inflammatory cytokines caused by exposure to automobile exhaust. The results showed that LHQWC reduced protein and mRNA expression of inflammatory cytokines in lung tissue by reducing blood levels of inflammatory cytokines, thus, protecting against lung tissue injury caused by automobile exhaust (Tang et al., 2015)."}

LitCovid-sentences

{"project":"LitCovid-sentences","denotations":[{"id":"T258","span":{"begin":0,"end":45},"obj":"Sentence"},{"id":"T259","span":{"begin":46,"end":244},"obj":"Sentence"},{"id":"T260","span":{"begin":245,"end":445},"obj":"Sentence"},{"id":"T261","span":{"begin":446,"end":532},"obj":"Sentence"},{"id":"T262","span":{"begin":533,"end":664},"obj":"Sentence"},{"id":"T263","span":{"begin":665,"end":682},"obj":"Sentence"},{"id":"T264","span":{"begin":683,"end":910},"obj":"Sentence"},{"id":"T265","span":{"begin":911,"end":1141},"obj":"Sentence"},{"id":"T266","span":{"begin":1142,"end":1300},"obj":"Sentence"},{"id":"T267","span":{"begin":1301,"end":1525},"obj":"Sentence"},{"id":"T268","span":{"begin":1526,"end":1726},"obj":"Sentence"},{"id":"T269","span":{"begin":1727,"end":1851},"obj":"Sentence"},{"id":"T270","span":{"begin":1852,"end":2166},"obj":"Sentence"},{"id":"T271","span":{"begin":2167,"end":2290},"obj":"Sentence"},{"id":"T272","span":{"begin":2291,"end":2415},"obj":"Sentence"},{"id":"T273","span":{"begin":2416,"end":2611},"obj":"Sentence"},{"id":"T274","span":{"begin":2612,"end":2797},"obj":"Sentence"},{"id":"T275","span":{"begin":2798,"end":3050},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Progress of Pharmacological Research on LHQWC\nModern pharmacological studies have shown that LHQWC has antiviral, immune-regulatory, anti-inflammatory, and antioxidant properties, efficacy against lung injury, and other effects (see Table 3 ).\nLHQWC significantly inhibited SARS-CoV-2 replication in Vero E6 cells and markedly reduced the production of pro-inflammatory cytokines (TNF-α, IL-6, CCL-2/MCP-1, and CXCL-10/IP-10) at the mRNA level. Furthermore, LHQWC treatment resulted in abnormal virion particle morphology in cells. LHQWC significantly inhibits SARS-CoV-2 replication, affects virus morphology and exerts anti-inflammatory activity in vitro (Li R. F. et al., 2020).\nIn vitro experiments have shown significant antiviral activity against SARS-CoV, AIV H7N9, dual H1N1/H3N2, together with inhibition of Middle East Respiratory Syndrome (MERS)-CoV activity to a certain degree (Yao et al., 2020). Yuewen Ding et al. used MTT and plaque reduction assays to show that LHQWC inhibited proliferation of multiple strains of influenza virus, and reduced virus titer and levels of inflammatory cytokines in the lungs of infected mice. The results indicated that LHQWC acted as a broad-spectrum antiviral and, in particular, regulated the immune response to viral infection (Ding et al., 2017). Qi Li et al. discovered that LHQWC not only reversed LPS-stimulated expression of macrophage chemotactic factor-1 (MCP-1) by macrophages, but also significantly improved pulmonary edema in a mouse model of acute lung injury. Inhibition of expression and secretion of MCP-1 in lung tissues of model mice was accompanied by reduced infiltration of mononuclear macrophages and reduction of inflammatory injury (Li et al., 2019). Fen Ping et al. studied the effects of LHQWC on rats with oxidative lung injury caused by fine particulate matters (PM 2.5). The results showed that LHQWC significantly reduced lactate dehydrogenase (LDH) and malondialdehyde (MDA) serum levels in rats with lung injury, increased levels of glutathione peroxidase (GSH-Px), reduced pathological damage of lung tissues, and inhibited exudation of inflammatory cells into the alveolar cavity. Together, the data indicated that LHQWC protected against oxidative stress injury in the lungs of rats (Ping et al., 2016). Wenwen Cui et al. studied the impact of LHQWC in a mouse model of acute lung injury caused by intratracheal infusion of LPS. LHQWC alleviated the inflammatory response in lung tissues by downregulating the IKK/IκB/nuclear factor (NF)-κB signaling pathway, thus, protecting mice from acute lung injury (Cui et al., 2016). Siwen Tang et al. studied the effects of LHQWC intervention on pathological lung tissue injury in mice and expression of inflammatory cytokines caused by exposure to automobile exhaust. The results showed that LHQWC reduced protein and mRNA expression of inflammatory cytokines in lung tissue by reducing blood levels of inflammatory cytokines, thus, protecting against lung tissue injury caused by automobile exhaust (Tang et al., 2015)."}

LitCovid-PD-HP

{"project":"LitCovid-PD-HP","denotations":[{"id":"T127","span":{"begin":1471,"end":1486},"obj":"Phenotype"},{"id":"T128","span":{"begin":1507,"end":1524},"obj":"Phenotype"},{"id":"T129","span":{"begin":2225,"end":2241},"obj":"Phenotype"},{"id":"T130","span":{"begin":2357,"end":2374},"obj":"Phenotype"},{"id":"T131","span":{"begin":2574,"end":2591},"obj":"Phenotype"}],"attributes":[{"id":"A127","pred":"hp_id","subj":"T127","obj":"http://purl.obolibrary.org/obo/HP_0100598"},{"id":"A128","pred":"hp_id","subj":"T128","obj":"http://www.orpha.net/ORDO/Orphanet_178320"},{"id":"A129","pred":"hp_id","subj":"T129","obj":"http://purl.obolibrary.org/obo/HP_0025464"},{"id":"A130","pred":"hp_id","subj":"T130","obj":"http://www.orpha.net/ORDO/Orphanet_178320"},{"id":"A131","pred":"hp_id","subj":"T131","obj":"http://www.orpha.net/ORDO/Orphanet_178320"}],"text":"Progress of Pharmacological Research on LHQWC\nModern pharmacological studies have shown that LHQWC has antiviral, immune-regulatory, anti-inflammatory, and antioxidant properties, efficacy against lung injury, and other effects (see Table 3 ).\nLHQWC significantly inhibited SARS-CoV-2 replication in Vero E6 cells and markedly reduced the production of pro-inflammatory cytokines (TNF-α, IL-6, CCL-2/MCP-1, and CXCL-10/IP-10) at the mRNA level. Furthermore, LHQWC treatment resulted in abnormal virion particle morphology in cells. LHQWC significantly inhibits SARS-CoV-2 replication, affects virus morphology and exerts anti-inflammatory activity in vitro (Li R. F. et al., 2020).\nIn vitro experiments have shown significant antiviral activity against SARS-CoV, AIV H7N9, dual H1N1/H3N2, together with inhibition of Middle East Respiratory Syndrome (MERS)-CoV activity to a certain degree (Yao et al., 2020). Yuewen Ding et al. used MTT and plaque reduction assays to show that LHQWC inhibited proliferation of multiple strains of influenza virus, and reduced virus titer and levels of inflammatory cytokines in the lungs of infected mice. The results indicated that LHQWC acted as a broad-spectrum antiviral and, in particular, regulated the immune response to viral infection (Ding et al., 2017). Qi Li et al. discovered that LHQWC not only reversed LPS-stimulated expression of macrophage chemotactic factor-1 (MCP-1) by macrophages, but also significantly improved pulmonary edema in a mouse model of acute lung injury. Inhibition of expression and secretion of MCP-1 in lung tissues of model mice was accompanied by reduced infiltration of mononuclear macrophages and reduction of inflammatory injury (Li et al., 2019). Fen Ping et al. studied the effects of LHQWC on rats with oxidative lung injury caused by fine particulate matters (PM 2.5). The results showed that LHQWC significantly reduced lactate dehydrogenase (LDH) and malondialdehyde (MDA) serum levels in rats with lung injury, increased levels of glutathione peroxidase (GSH-Px), reduced pathological damage of lung tissues, and inhibited exudation of inflammatory cells into the alveolar cavity. Together, the data indicated that LHQWC protected against oxidative stress injury in the lungs of rats (Ping et al., 2016). Wenwen Cui et al. studied the impact of LHQWC in a mouse model of acute lung injury caused by intratracheal infusion of LPS. LHQWC alleviated the inflammatory response in lung tissues by downregulating the IKK/IκB/nuclear factor (NF)-κB signaling pathway, thus, protecting mice from acute lung injury (Cui et al., 2016). Siwen Tang et al. studied the effects of LHQWC intervention on pathological lung tissue injury in mice and expression of inflammatory cytokines caused by exposure to automobile exhaust. The results showed that LHQWC reduced protein and mRNA expression of inflammatory cytokines in lung tissue by reducing blood levels of inflammatory cytokines, thus, protecting against lung tissue injury caused by automobile exhaust (Tang et al., 2015)."}

LitCovid-PubTator

2_test

{"project":"2_test","denotations":[{"id":"32848729-32205232-39628374","span":{"begin":676,"end":680},"obj":"32205232"},{"id":"32848729-28235408-39628375","span":{"begin":1294,"end":1298},"obj":"28235408"},{"id":"32848729-28065220-39628376","span":{"begin":2284,"end":2288},"obj":"28065220"}],"text":"Progress of Pharmacological Research on LHQWC\nModern pharmacological studies have shown that LHQWC has antiviral, immune-regulatory, anti-inflammatory, and antioxidant properties, efficacy against lung injury, and other effects (see Table 3 ).\nLHQWC significantly inhibited SARS-CoV-2 replication in Vero E6 cells and markedly reduced the production of pro-inflammatory cytokines (TNF-α, IL-6, CCL-2/MCP-1, and CXCL-10/IP-10) at the mRNA level. Furthermore, LHQWC treatment resulted in abnormal virion particle morphology in cells. LHQWC significantly inhibits SARS-CoV-2 replication, affects virus morphology and exerts anti-inflammatory activity in vitro (Li R. F. et al., 2020).\nIn vitro experiments have shown significant antiviral activity against SARS-CoV, AIV H7N9, dual H1N1/H3N2, together with inhibition of Middle East Respiratory Syndrome (MERS)-CoV activity to a certain degree (Yao et al., 2020). Yuewen Ding et al. used MTT and plaque reduction assays to show that LHQWC inhibited proliferation of multiple strains of influenza virus, and reduced virus titer and levels of inflammatory cytokines in the lungs of infected mice. The results indicated that LHQWC acted as a broad-spectrum antiviral and, in particular, regulated the immune response to viral infection (Ding et al., 2017). Qi Li et al. discovered that LHQWC not only reversed LPS-stimulated expression of macrophage chemotactic factor-1 (MCP-1) by macrophages, but also significantly improved pulmonary edema in a mouse model of acute lung injury. Inhibition of expression and secretion of MCP-1 in lung tissues of model mice was accompanied by reduced infiltration of mononuclear macrophages and reduction of inflammatory injury (Li et al., 2019). Fen Ping et al. studied the effects of LHQWC on rats with oxidative lung injury caused by fine particulate matters (PM 2.5). The results showed that LHQWC significantly reduced lactate dehydrogenase (LDH) and malondialdehyde (MDA) serum levels in rats with lung injury, increased levels of glutathione peroxidase (GSH-Px), reduced pathological damage of lung tissues, and inhibited exudation of inflammatory cells into the alveolar cavity. Together, the data indicated that LHQWC protected against oxidative stress injury in the lungs of rats (Ping et al., 2016). Wenwen Cui et al. studied the impact of LHQWC in a mouse model of acute lung injury caused by intratracheal infusion of LPS. LHQWC alleviated the inflammatory response in lung tissues by downregulating the IKK/IκB/nuclear factor (NF)-κB signaling pathway, thus, protecting mice from acute lung injury (Cui et al., 2016). Siwen Tang et al. studied the effects of LHQWC intervention on pathological lung tissue injury in mice and expression of inflammatory cytokines caused by exposure to automobile exhaust. The results showed that LHQWC reduced protein and mRNA expression of inflammatory cytokines in lung tissue by reducing blood levels of inflammatory cytokines, thus, protecting against lung tissue injury caused by automobile exhaust (Tang et al., 2015)."}

PMC:7396557 / 33353-36403 JSONTXT

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PMC:7396557 / 33353-36403 JSON TXT