Oxymatrine is one of the alkaloids extracted from Chinese herb Sophora japonica (Sophora flavescens Ait.) with activities of anti-inflammation, inhibiting immune reaction, antivirus, protecting hepatocytes and antihepatic fibrosis. However, the effect of oxymatrine on acute lung injury (ALI) has not been known yet. In this study, the effect of oxymatrine on ALI was investigated using an oleic acid-induced ALI mouse model. Morphological findings showed that the oleic acid group demonstrated a marked lung injury represented by prominent atelectasis, intraalveolar and interstitial patchy hemorrhage, edema, thickened alveolar septum, formation of hyaline membranes and the existence of inflammatory cells in alveolar spaces. While in the oxymatrine/dexamethasone group, these changes were less severe and in the vicinity of the control group. Furthermore, pretreatment with oxymatrine significantly alleviated oleic acid-induced lung injury accompanied by reduction of lung index and wet-to-dry weight ratio, decreases in serum TNF-alpha level and inhibition of phosphorylated p38 MAPK. These findings suggest that oxymatrine has a beneficial effect on acute lung injury induced by oleic acid in mice and may inhibit the production of proinflammatory cytokine, TNF-alpha, by means of the inhibition of p38 MAPK.
Coronavirus disease 2019 (COVID-19) emerged in Wuhan and rapidly spread throughout the world in December 2019. The present study aimed to describe the clinical characteristics and laboratory findings of 78 patients with COVID-19 in order to enhance the understanding of the disease. Medical records and data of 78 patients with COVID-19, including demographics, clinical features, laboratory findings and radiological characteristics, were collected and analyzed. Of the 78 hospitalized patients with COVID-19, the median age was 66.5 years and 48.7% of patients were male. Hypertension and diabetes were the most common chronic underlying diseases, and the most common symptoms were a cough and a fever. Furthermore, the most common findings on the chest CT were extensive ground-glass opacity and bilateral shadowing. Anemia and lymphocytopenia were the most common abnormalities identified during routine blood tests. COVID-19 caused early liver renal damage, with 52.9% of patients displaying elevated D-dimer levels, 98.7% of patients displaying elevated IL-6 levels and 80.8% of patients displaying a reduced level of low-density lipoprotein cholesterol (LDL-C). In the present single-center case study of 78 patients with COVID-19 in Wuhan, China, the patients displayed abnormal routine blood tests, liver function, renal function and levels of D-dimer, LDL-C and IL-6. Therefore, the development of drugs and vaccines that can be used to prevent and treat infections of COVID-19 is urgently required.
No prognostic tools for the prediction of COVID-19 pneumonia severity and mortality are available. We explored whether CURB-65, PSI, and APACHE-II could predict COVID-19 pneumonia severity and mortality. We included 167 patients with confirmed COVID-19 pneumonia in this retrospective study. The severity and 30-day mortality of COVID-19 pneumonia were predicted using PSI, CURB-65, and APACHE-II scales. Kappa test was performed to compare the consistency of the three scales. There was a significant difference in the distribution of the scores of the three scales ( P < 0.001). Patients with PSI class ⩽III, CURB-65 ⩽1, and APACHE-II-I all survived. The ROC analysis showed the areas under the curve of the PSI, CURB-65, and APACHE-II scales were 0.83 (95% CI, 0.74–0.93), 0.80 (95% CI, 0.69–0.90), and 0.83 (95% CI, 0.75–0.92), respectively. Our findings suggest that PSI and CURB-65 might be useful to predict the severity and mortality of COVID-19 pneumonia.
Introduction: Lysyl hydroxylase 3 (LH3) is a collagen post-translational modifying enzyme; it is abnormally activated during the formation of collagen cross-links. iCRT3 is an inhibitor of both Wnt and β-catenin responsive transcription. We hypothesized that LH3 is regulated by TGFβ1/Smad3 signaling and Wnt/β-catenin signaling pathways. Some evidence suggested that there is complicated cross-talk between the two signal pathways in the genesis of pulmonary fibrosis. Material and methods: The normal culturing human lung cancer cell line A549 was derived from pulmonary epithelial cells. Transforming growth factor-β1 (TGF-β1) was induced A549 cells of pulmonary fibrosis. MTT assays detected cell growth stimulation by TGF-β1; collagen pyridine-crosslinking contents were detected by ELISA kits. Immunofluorescence were used to evaluate expression of key molecules in PLOD3 (LH3), Wnt/β-catenin and TGFβ1/Smad3 pathways. Results: Our findings suggested that iCRT3 could decrease LH3 protein expression (p < 0.01), Wnt1, β-catenin and p-Smad3 protein expression (p < 0.05). Knock-down PLOD3 could decrease LH3, collagen I gene and protein expression (p < 0.05). These effects were associated with decreasing collagen pyridine-crosslinking production (p < 0.05). However, ovexpression PLOD3 could increase LH3, collagen I gene and protein expression (p < 0.05). The result showed that LH3 plays an important role in collagen post-translational modifications, and it is regulated by Wnt/β-catenin and TGFβ1/ Smad3 pathways. Conclusions: This study suggests that PLOD3 (LH3) represents a target to prevent pulmonary fibrosis.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.