RESUMEN
BACKGROUND: Emodin is a traditional medicine that has been shown to exert anti-inflammatory and anti-oxidative effects. Previous research has indicated that emodin can alleviate myocardial remodeling and inhibit myocardial hypertrophy and fibrosis. However, the mechanism by which emodin affects myocardial fibrosis (MF) has not yet been elucidated. METHODS: Fibroblasts were treated with ANGII, and a mouse model of MF was established by ligation of the left anterior descending coronary artery. Cell proliferation was examined by a Cell Counting Kit-8 (CCK8) assay. Dihydroethidium (DHE) was used to measure reactive oxygen species (ROS) levels, and Masson and Sirius red staining were used to examine changes in collagen fiber levels. PI3K was over-expressed by lentiviral transfection to verify the effect of emodin on the PI3K/AKT/mTOR signaling axis. Changes in cardiac function in each group were examined by echocardiography. RESULTS: Emodin significantly inhibited fibroblast proliferation, decreased intracellular ROS levels, significantly upregulated collagen II expression, downregulated α-SMA expression, and inhibited PI3K/AKT/mTOR pathway activation in vitro. Moreover, the in vivo results were consistent with the in vitro. Emodin significantly decreased ROS levels in heart tissue and reduced collagen fibrillogenesis. Emodin could regulate the activity of PI3K to increase the expression of collagen II and downregulate α-SMA expression in part through the PI3K/AKT/mTOR pathway, and emodin significantly improved cardiac structure and function in mice. CONCLUSIONS: This study revealed that emodin targeted the PI3K/AKT/mTOR pathway to inhibit the development of myocardial fibrosis and may be an antifibrotic agent for the treatment of cardiac fibrosis.
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Emodina , Proteínas Proto-Oncogénicas c-akt , Ratones , Animales , Proteínas Proto-Oncogénicas c-akt/metabolismo , Emodina/farmacología , Especies Reactivas de Oxígeno , Fosfatidilinositol 3-Quinasas/metabolismo , Serina-Treonina Quinasas TOR/metabolismo , Fibrosis , ColágenoRESUMEN
Purpose: Dispelling dampness, relieving turbidity and dredging collaterals decoction (DED), is a traditional Chinese medicine used in the treatment of hyperuricemia. We aimed to explore the effect and mechanism of DED in the treatment of hyperuricemia. Methods: The effects of DED (9.48, 4.74, and 2.37 g/kg/d) on potassium oxonate (750 mg/kg/d)-induced hyperuricemia in rats were evaluated by serum uric acid (UA), creatinine (CRE), blood urea nitrogen (BUN), and renal pathological changes. Network pharmacology was used to identify the effective components and targets of DED, and the key targets and signaling pathways for its effects on hyperuricemia were screened. Molecular docking was used to predict the action of DED. H&E, immunohistochemistry, WB, and PCR were used to validate the network pharmacology results. Results: DED can effectively alleviate hyperuricemia, inhibit UA, CRE, BUN, and xanthine oxidase (XOD) activity, and reduce renal inflammatory cell infiltration and glomerular atrophy. The experiment identified 27 potential targets of DED for hyperuricemia, involving 9 components: wogonin, stigmasterol 3-O-beta-D-glucopyranoside, 3ß-acetoxyatractylone, beta-sitosterol, stigmasterol, diosgenin, naringenin, astilbin, and quercetin. DED can relieve hyperuricemia mainly by inhibiting RAGE, HMGB1, IL17R, and phospho-TAK1, and by regulating the AGE-RAGE and IL-17 signaling pathways. Conclusion: DED can alleviate hyperuricemia by inhibiting XOD activity and suppressing renal cell apoptosis and inflammation via the AGE-RAGE signaling pathway and IL-17 signaling pathway. This study provides a theoretical basis for the clinical application of DED.
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Hiperuricemia , Ratas , Animales , Hiperuricemia/inducido químicamente , Hiperuricemia/tratamiento farmacológico , Interleucina-17/metabolismo , Ácido Úrico , Simulación del Acoplamiento Molecular , Riñón , Xantina Oxidasa/metabolismo , Xantina Oxidasa/farmacologíaRESUMEN
Aflatoxin B1 (AFB1) is one of the most commonly found mycotoxin in corn, which is highly toxic, carcinogenic, teratogenic, and mutagenic for the health of humans and animals. In order to reduce the AFB1 in corn, corn kernels were processed with Water-assisted Microwaves Treatment (WMT) and the feasibility of WMT processing on AFB1 reduction and its effects on corn quality were analyzed. Increasing the treatment time and microwave power could increase the reduction of AFB1, and the maximum reduction rate could reach 58.6% and 56.8%, respectively. There was no significant correlation between the initial concentration of AFB1 and the reduction rate of AFB1. During WMT, the main toxigenic molds were sterilized completely, and the moisture content of corn climbed up and then declined to the initial level. WMT could obviously increase the fatty acid value and pasting temperature of corn and reduce the all paste viscosity of corn. However, it had little effect on the color of corn. The results indicated that WMT could reduce AFB1 effectively and avoid the vast appearance of heat-damaged kernels simultaneously. Undoubtedly, water played an important role in WMT. This result provides a new idea for the reduction of AFB1 by microwave.
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Aflatoxina B1/análisis , Aspergillus flavus/metabolismo , Microondas , Valor Nutritivo , Pasteurización , Agua/química , Zea mays/microbiología , Aflatoxina B1/toxicidad , Color , Ácidos Grasos/análisis , Estudios de Factibilidad , Microbiología de Alimentos , Factores de Tiempo , ViscosidadRESUMEN
CONTEXT: Despite the abundance of knowledge regarding high-altitude pulmonary edoema (HAPE) and high-altitude pulmonary hypertension (HAPH), their prevalence continues to be on the rise. Thus, there is an urgent need for newer safe, effective, and relatively economic drug candidates. China is particularly known for the use of medicinal plants. OBJECTIVE: This review summarizes the medicinal plants used for HAPE and HAPH in the past 30 years, as well as some potential plants. METHODS: Publications on HAPE and HAPH from 1990 to 2020 were identified using Web of Science, PubMed, SCOPUS, Springer Link, Google Scholar databases, Chinese Clinical Trial Registry and CNKI with the following keywords: 'medicinal plants,' 'hypoxia,' 'high altitude pulmonary edema,' 'high altitude pulmonary hypertension,' 'pathophysiology,' 'mechanisms,' 'prevention,' 'treatment,' 'human,' 'clinical,' 'safety,' and 'pharmacokinetics.' RESULTS: We found 26 species (from 20 families) out of 5000 plants which are used for HAPE and HAPH prevention or treatment. Rhodiola rosea Linn. (Crassulaceae) is the most widely utilized. The most involved family is Lamiaceae, which contains 5 species. DISCUSSION AND CONCLUSIONS: We mainly reviewed the medicinal plants and mechanisms for the treatment of HAPE and HAPH, and we also assessed related toxicology experiments, pharmacokinetics and bioavailability. Potential medicinal plants were also identified. Further research is needed to determine the pharmacological effects and active ingredients of these potential medicinal plants.
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Hipertensión Pulmonar/tratamiento farmacológico , Extractos Vegetales/farmacología , Edema Pulmonar/tratamiento farmacológico , Altitud , Animales , Pueblo Asiatico , Disponibilidad Biológica , Humanos , Ratones , Plantas Medicinales , RatasRESUMEN
The polyprenols and their derivatives are highlighted in this study. These lipid linear polymers of isoprenoid residues are widespread in nature from bacteria to human cells. This review primarily presents the synthesis and biological activities of polyprenyl derivatives. Attention is focused on the synthesis and biological activity of dolichols, polyprenyl ester derivatives and polyprenyl amines. Other polyprenyl derivatives, such as oxides of polyprenols, aromatic polyprenols, polyprenyl bromide and polyprenyl sulphates, are mentioned. It is noted that polyprenyl phosphates and polyprenyl-linked glycosylation have better antibacterial, gene therapy and immunomodulating performance, whereas polyprenyl amines have better for antibacterial and antithrombotic activity. Dolichols, polyprenyl acetic esters, polyprenyl phosphates and polyprenyl-linked glycosylation have pharmacological anti-tumour effects. Finally, the postulated prospect of polyprenols and their derivatives are discussed. Further in vivo studies on the above derivatives are needed. The compatibility of polyprenols and their derivatives with other drugs should be studied, and new preparations of polyprenyl derivatives, such as hydrogel glue and release-controlled drugs, are suggested for future research and development.