Search

Some domestic scholars revealed the effectiveness of Wenshen Yiqi Keli (WSYQKL) on chronic obstructive pulmonary disease (COPD). However, the exact mechanism of WSYQKL on COPD is fuzzy and needs further research. We adopted UPLC-Q/TOF-MS to analyze the chemical components of WSYQKL. In in vitro experiments, human airway smooth muscle cells (hASMCs) were intervened with 2.5% cigarette smoke extract (CSE), medicine serum of WSYQKL, miR-155 mimic, and FoxO3a silencing. Cell viability, proliferation, migration, and the expressions of miR-155, PCNA, Ki67, p21, p27, and FoxO3a were examined by cell counting kit-8, EdU staining, Transwell assay, scarification assay, qRT-PCR, immunol cytochemistry, and western blot, respectively. The association between miR-155 and FoxO3a was assessed by database and luciferase reporter gene analysis. We identified 47 kinds of chemical compositions of WSYQKL in ESI+ mode and 42 kinds of components of WSYQKL in ESI− mode. The medicine serum of WSYQKL strongly alleviated the proliferation and migration of hASMCs induced by CSE in a concentration-dependent manner. The medicine serum of WSYQKL enhanced the levels of p21, p27, and FoxO3a and weakened PCNA and Ki67 levels in hASMCs induced by CSE with the increase of concentration. MiR-155 mimic or FoxO3a silencing notably advanced CSE-treated HASMC viability, proliferation, migration, and the levels of PCNA and Ki67 and downregulated the levels of p21, p27, and FoxO3a in CSE-triggered hASMCs, which was reversed by WSYQKL-containing serum. Our results described that WSYQKL alleviated the proliferation and migration of hASMCs induced by CSE by modulating the miR-155/FoxO3a axis. [ABSTRACT FROM AUTHOR]

Objective. The objective of this study was to observe the protective effect of Rhodiola wallichiana drops in a rat model of fine particulate matter (PM2.5) lung injury. Methods. Forty male Wistar rats were randomly divided into blank control (NC), normal saline (NS), PM2.5-infected (PM), and Rhodiola wallichiana (RW) groups. Rats in the NC group were not provided any interventions, whereas those in the NS and PM groups were administered normal saline and PM2.5 suspension by trachea drip once a week for four weeks. Rats in the RW group were intraperitoneally administered Rhodiola wallichiana for 14 days and then administered PM2.5 suspension by trachea drip 7 days after drug delivery. The levels of inflammatory factors such as interleukin-6, interleukin-1β, and tumor necrosis factor-alpha and oxidative stress biomarkers such as 8-hydroxy-2′-deoxyguanosine, 4-hydroxynonenal, and protein carbonyl content were determined in the serum and bronchoalveolar lavage fluid by ELISA. The level of 4-hydroxynonenal in the lung was also determined using Western blotting and immunohistochemical staining. Results. Levels of inflammatory factors and oxidative stress biomarkers were all increased in the PM group but decreased in the RW group. Western blotting revealed increased 4-hydroxynonenal levels in the PM group but decreased levels in the RW group. Immunohistochemical staining also provided similar results. Conclusion. Rhodiola wallichiana could protect rats from inflammation and oxidative stress injury caused by PM2.5. [ABSTRACT FROM AUTHOR]

At present, the global prevalence of peripheral arterial disease is increasing year by year, and it has become a worldwide disease. Studies have shown that transplanting endothelial progenitor cells (EPCs) into ischemic tissues can improve the tissue ischemia, thereby having a therapeutic effect on peripheral arterial diseases. This indicates that EPCs play a therapeutic effect in peripheral arterial disease. Recent studies have shown that peptidylarginine deiminase (PAD) is involved in the regulation of epigenetics and its inhibitor Cl-amidine can improve endothelium-dependent vasodilation and significantly reduce the formation of arterial thrombosis. It can also play a role in hematopoietic stem cells that share the same origin with EPCs. Therefore, we speculate that PAD4 may also have an effect on EPCs through a similar mechanism, thereby participating in the damage and repair of peripheral arterial disease. Therefore, we first detected the expression of PAD4 in EPCs of peripheral arterial disease and detected changes in the number and function of endothelial progenitor cells in peripheral blood after injecting the PAD4 inhibitor Cl-amidine into mice. A mouse model of lower limb ischemia was established to explore the effect of PAD4 on the function of EPCs in peripheral arterial disease. The results show that PAD4 is highly expressed in peripheral arterial diseases and the PAD4 inhibitor Cl-amidine can increase the number of EPCs and can treat peripheral arterial diseases by improving the proliferation, migration, and vascularization of EPCs. [ABSTRACT FROM AUTHOR]

Objectives. Fatty liver disease (FLD) is a major cause of morbidity and mortality worldwide. Dietary cholesterol and alcohol consumption are important risk factors for the progression of FLD, but whether and how alcohol induces more severe FLD with cholesterol ingestion remain unclear. Herein, we mainly used the Lieber-DeCarli diet to establish the FLD mouse model to investigate the synergistic effects of alcohol and cholesterol metabolism on liver damage. The indices of aspartate transaminase (AST), alanine transaminase (ALT), low-density lipoprotein cholesterol (LDL-c), and total cholesterol (TC) levels, inflammation foci, and pathogenesis by hematoxylin and eosin (H&E) and Oil Red O staining revealed that alcohol induces more severe liver damage by influencing cholesterol metabolism, which might be primarily related to the influence of cholesterol absorption, synthesis, and excretion on the liver or small intestine. Moreover, inhibition of absorption of intestinal cholesterol, but not of fat, sucrose, and alcohol, absorption into the body's metabolism by Ezetimibe, significantly improved FLD in rats fed with the high fat-cholesterol-sucrose and alcohol diet. These results showed that alcohol plays an important role in cholesterol metabolism in FLD. [ABSTRACT FROM AUTHOR]