Gastrointestinal hemorrhage from angiodysplasiamay may be associated with degenerative aortic valve stenosis , the associated of the two conditions termed Heyde ’ s syndrome.Gastrointestinal angiodysplasia and aortic valve stenosis areboth chronic degenerative diseases, and the incidence rate increased with age.Degenerative aortic stenosis can enhance high molec-ular weight polymer damage, which subsequently increases the risk of gastrointestinal bleeding.Aortic valve replacement is considered as the first-line treatment for patients with severe aortic stenosis , and can effectively improve the outcomes of hemor-rhagic angiodysplasia and acquired coagulopathy .However, the substantial connection between aortic valve stenosis and gastro-intestinal bleeding remains unclear, and the clinical diagnosis and treatment of this syndrome need more evidences.Herein, we will review the knowledge of epidemiology, pathogenesis and clinical diagnosis and treatment of Heyde’ s syndrome.

The outbreak of COVID-19 posed a huge threat to human health and social stability. With the rapid spread of the virus around the world, the drug development and related research of novel coronavirus (SARS-CoV-2) have become an urgent issue in the medical field. COVID-19 fails into the category of epidemics in the theory of TCM. LHQW capsule has repeatedly played an important role in many major epidemics. Previous studies have shown that LHQW capsule can inhibit the biological activity of varied viruses including MERS-CoV and SARS-CoV. The paper summarizes the relevant research data and achievements of LHQW capsule in the past few years, reviews the chemical constituents, clinical efficacy and pharmacological effects of LHQW capsule, and provides scientific basis for the anti-virus mechanism of LHQW capsule and clinical treatment of COVID-19.

OBJECTIVE To study the effect and potential mechanism of eriodictyol on non-alcoholic fatty liver disease （NAFLD）. METHODS Sixteen C57BL/6J mice were randomly divided into control group， NAFLD model group， and eriodictyol low-dose and high-dose groups （50， 100 mg/kg）， with 4 mice in each group. Except for control group， the other groups were fed with high fat diet to induce NAFLD model. After four weeks of preprocessing， they were given relevant medicine intraperitoneally （0.01 mL/g）， once a day， for 6 consecutive weeks. The body weight and liver weight of mice were measured， and the pathological damage of liver tissue in mice was observed. The levels of aspartate aminotransferase （AST）， alanine aminotransferase（ALT）， and triglycerides （TG） in serum， as well as the protein expressions of nuclear factor-erythroid 2-related factor 2 （Nrf2） and heme oxygenase-1 （HO-1） in liver tissue were determined. In vitro NAFLD model was established by using 0.5 mmol/L oleic acid （OA） in HepG2 cells. Normal control group， NAFLD model group and eriodictyol low-， medium- and high-concentration groups （50， 100， 150 μmol/L） were set up. HepG2 cells in drug groups were treated with eriodictyol for 24 h at the time of modeling. The lipid deposition was observed in cells， and the levels of TG， malondialdehyde （MDA） and reactive oxygen species （ROS） as well as the phosphorylation levels of the mitogen-activated protein kinase （MAPK） signal pathway related proteins [extracellular signal-regulated kinase （ERK）， c- Jun N-terminal kinase （JNK）] and the protein expressions of Nrf2 and HO-1 were all determined. RESULTS In the in vivo experiment， compared with the NAFLD model group， the body weight， liver weight， the serum levels of AST， ALT and TG were all decreased significantly in eriodictyol low- and high-dose groups （except for serum level of AST in eriodictyol low-dose group） （P＜0.01）； liver lipid deposition was reduced significantly and the protein expressions of Nrf2 and HO-1 in liver tissues were further up-regulated （P＜0.01）. In the in vitro experiment， compared with the NAFLD model group， the lipid deposition in hepatocytes was reduced in eriodictyol low-， medium- and high-concentration groups （P＜0.01）， and the levels of ROS， MDA and TG were down-regulated （P＜0.05 or P＜0.01）； the phosphorylation levels of ERK and JNK were significantly down-regulated （P＜0.01）， while the protein expressions of Nrf2 and HO-1 were up-regulated significantly （P＜0.01）. CONCLUSIONS Eriodictyol can inhibit MAPK signaling pathway and activate Nrf2/HO-1 signaling pathway to alleviate NAFLD.