Objectives To explore the association between CT-derived pectoralis muscle index (PMI) and COVID-19 induced lung injury. Methods We enrolled 116 elderly COVID-19 patients linked to the COVID-19 outbreak in Nanjing Lukou international airport. We extracted three sessions of their CT data, including one upon admission (T1), one during the first 2 weeks when lung injury peaked (T2) and one on day 14 ± 2 (T3). Lung injury was assessed by CT severity score (CTSS) and pulmonary opacity score (POS). Pneumonia evolution was evaluated by changes of CT scores at T2 from T1(Δ). Results The maximum CT scores in low PMI patients were higher than those of normal PMI patients, including CTSS1 (7, IQR 6–10 vs. 5, IQR 3–6, p < 0.001), CTSS2 (8, IQR 7–11 vs. 5, IQR 4–7, p < 0.001) and POS (2, IQR 1–2.5 vs. 1, IQR 1–2, p < 0.001). Comorbidity (OR = 6.15, p = 0.023) and the presence of low PMI (OR = 5.43, p = 0.001) were predictors of lung injury aggravation with ΔCTSS1 > 4. The presence of low PMI (OR = 5.98, p < 0.001) was the predictor of lung injury aggravation with ΔCTSS2 > 4. Meanwhile, presence of low PMI (OR = 2.82, p = 0.042) and incrementally increasing D-dimer (OR = 0.088, p = 0.024) were predictors of lung injury aggravation with ΔPOS = 2. Conclusions PMI can be easily assessed on chest CT images and can potentially be used as one of the markers to predict the severity of lung injury in elderly COVID-19 patients.
Objective. Atherosclerosis is a chronic inflammatory disease, which is closely related to hyperlipidemia, inflammatory responses, and oxidative stress. As natural products, polydatin (PD) and Polygonatum sibiricum polysaccharides (PSP) have remarkable pharmacological effects in anti-inflammatory, antioxidant stress, and lipid regulation. In this study, we sought to investigate whether the combination of polydatin and P. sibiricum polysaccharides play an anti-atherosclerotic role in alleviating inflammatory responses by inhibiting the toll-like receptor4 (TLR4)/myeloid differentiation factor88(MyD88)/nuclear factor-kappa B(NF-κB) signaling pathway. Methods. Thirty-two ApoE-/- mice were fed with a high-fat diet (HFD) starting at the age of 8 weeks. Mice were randomly divided into four groups; (1) model group, (2) PD (100 mg/kg) + PSP (50 mg/kg) group, (3) TAK-242 (3 mg/kg) (TLR4 inhibitor) group, (4) PD (100 mg/kg) + PSP (50 mg/kg) + TAK-242 (3 mg/kg) group. Eight age-matched wild-type C57BL/6J mice fed an ordinary diet were used as a control group. Blood lipid levels were measured with an automatic biochemical analyzer. The lipid accumulation and histopathological changes in the aorta and liver were observed by Oil Red O and hematoxylin and eosin (H&E) staining, respectively. ELISA was performed to measure the serum levels of vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1). Western blot analysis was performed to analyze the expression of key proteins in the TLR4/MyD88/NF-κB signaling pathway. Results. Compared with the model group, the combination of PD and PSP significantly inhibit serum lipids (low-density lipoprotein cholesterol, total cholesterol, and triglyceride) and cell adhesion molecules (VCAM-1, ICAM-1). Oil Red O staining indicated that the combination of PD and PSP decrease lipid accumulation in the aorta and liver. Moreover, H&E staining suggested that the combination of PD and PSP alleviate aortic intimal hyperplasia, inflammatory cell infiltration, and hepatic steatosis. Finally, the combination of PD and PSP inhibit the expression of TLR4, MyD88, and the phosphorylation level of NF-κB p65 protein in the aorta. Conclusions. Polydatin synergizes with P. sibiricum polysaccharides in preventing the development of atherosclerosis in ApoE–/– mice by inhibiting the TLR4/MyD88/NF-κB signaling pathway.
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