| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T433 |
0-44 |
Sentence |
denotes |
Progress of Pharmacological Research on TRQI |
| T434 |
45-234 |
Sentence |
denotes |
Modern pharmacological studies have shown that TRQI is effective against influenza virus, destroys bacterial biofilm, inhibits airway inflammation, and improves lung injury (see Table 3 ). |
| T435 |
235-443 |
Sentence |
denotes |
Research by Jinsu Zheng et al. discovered that TRQI improved pathological injury of lung tissues in mice infected with influenza virus, and had significant antiviral activity in influenza virus infected mice. |
| T436 |
444-581 |
Sentence |
denotes |
The antiviral activity of TRQI might be due to its inhibition of cellular proliferation and enhancement of immunity (Zheng and Gu, 2009). |
| T437 |
582-717 |
Sentence |
denotes |
Weifeng Yang et al. discovered that TRQI could destroy methicillin-resistant Staphylococcus aureus (MRSA) biofilm and induce its death. |
| T438 |
718-949 |
Sentence |
denotes |
When combined with vancomycin or linezolid below the minimal inhibitory concentration (MIC) concentration, synergistic anti-biofilm activity was observed that was significantly higher than when using TRQI alone (Yang et al., 2018). |
| T439 |
950-1169 |
Sentence |
denotes |
Research by Yi Wang et al. showed that the efficacy of TRQI in the treatment of acute pneumonia was mediated by destruction of bacterial biofilm, which is different to the mechanism of penicillin (Wang Y. et al., 2011). |
| T440 |
1170-1339 |
Sentence |
denotes |
Wei Liu et al. discovered that TRQI might treat airway mucus hypersecretion by regulating the interleukin-17 (IL-17) signaling pathway and its downstream protein MUC5AC. |
| T441 |
1340-1574 |
Sentence |
denotes |
An in vivo experiment showed that TRQI could significantly inhibit excessive secretion of LPS-stimulated MUC5AC and expression of TNF-α, interleukin-6 (IL-6), IL-8, and IL-17A in terms of protein and mRNA levels (Liu W. et al., 2019). |
| T442 |
1575-1769 |
Sentence |
denotes |
Animal experiments conducted by Wei Liu et al. showed that TRQI inhibited airway inflammation caused by LPS through the MAPK/NF-κB pathway, and showed a dose-dependent effect (Liu et al., 2016). |
| T443 |
1770-2012 |
Sentence |
denotes |
Li Wen et al. found that TRQI improved signs and symptoms in AECOPD patients, which might be mediated by reduction of serum IL-8 and neutrophil elastase (NE) levels, and improved airway inflammation and mucus hypersecretion (Li et al., 2010). |
| T444 |
2013-2342 |
Sentence |
denotes |
Research by Li Pengtao et al. discovered that TRQI improved blood flow in capillaries of the alveolar walls while repressing the LPS-induced inflammatory cascade, which was the pharmacological basis for its effective alleviation of acute lung injury and prevention of decreased arterial partial oxygen pressure (Li et al., 2005). |
