RESUMEN

OBJECTIVES: Asthma is a heterogeneous disease characterized by chronic airway inflammation. Huashanshen dripping pills (HSS) are commonly utilized for relieving asthma, relieving cough, and expelling phlegm. At present, the molecular mechanism against airway inflammation remains unclear. METHODS: In this study, network pharmacology, molecular docking technology, and molecular dynamic simulation were used to predict the therapeutic pathways of HSS for asthma. The ovalbumin-induced mouse model was used to further validate the prediction by RT-qPCR, western blot, immunofluorescence, and related methods. KEY FINDINGS: The findings indicate that HSS improves lung function and relieves lung inflammation by reducing inflammatory cell infiltration around the bronchus and reducing eosinophilic counts in bronchoalveolar lavage fluid (BALF). In addition, it lowers the levels of inflammatory cytokines and the expression levels of interleukin-4, interleukin-5, and interleukin-13 mRNA. HSS also inhibits the phosphorylation and nuclear translocation of NF-κB p65 protein. CONCLUSIONS: All results suggested that HSS can decrease airway inflammation in asthmatic mice by inhibiting NF-κB signaling pathway. This finding will shed light on how it can be used to treat asthma.

RESUMEN

BACKGROUND: Astragaloside IV has emerged as a pharmaceutical monomer with great medical applications and potential. Astragaloside IV has many effects such as improving myocardial ischemia, cerebral ischemia-reperfusion injury, anti-inflammatory, analgesic, antiviral, promoting lymphocyte proliferation, and antitumor effects. However, there are few bibliometric studies on astragaloside IV. OBJECTIVES: We aim to visualize the hotspots and trends in astragaloside IV research through bibliometric analysis to further understand the future development of basic and clinical research. Methods The articles and reviews on astragaloside IV were screened from the Web of Science Core Collection, and knowledge maps were generated using CiteSpace software. Bibliometric analysis was performed on 971 articles published from 1998 to 2022. RESULTS: The number of articles on astragaloside IV increased yearly. These publications came from 42 countries/regions, with China being the largest. The primary research institutions were Shanghai University of Traditional Chinese Medicine and Guangzhou University of Traditional Chinese Medicine. Journal of Ethnopharmacology was the most studied journal and co-cited journal. A total of 473 authors were included, among which Hongxin Wang had the highest number of publications and Zhang Wd had the highest total citation frequency. After analysis, the most common keywords are astragaloside IV, expression, and oxidative stress. Cardiovascular disease, cerebral ischemia, cancer, and kidney disease are current and developing research fields. CONCLUSION: This study used bibliometrics and visualization methods to analyze the research hotspots and trends of astragaloside IV. Astragaloside IV on ischemia-reperfusion injury, cancer, and tumor may become the focus of future research.

Asunto(s)

RESUMEN

Neonatal hypoxic-ischemic brain damage (HIBD) is one of the main causes of neonatal acute death and chronic nervous system impairment, but still lacks effective treatments. ZNF580/ZFP580, reported in our previous studies, may be a newly identified member of the Krüppel-like factor (KLF) family, and has anti-apoptotic effects during ischemic myocardial injury. In the present study, we showed that the expression levels of both ZFP580/ZNF580 mRNA and protein increased significantly in neonatal HIBD rats and oxygen-glucose deprivation (OGD) SH-SY5Y cell models. ZNF580 overexpression promoted neuron survival and suppressed neuron apoptosis after OGD in neuron-like SH-SY5Y cells, while interference with ZNF580 resulted in the opposite results. RNA-seq analysis identified 248 differentially-expressed genes (DEGs) between ZNF580 overexpression SH-SY5Y cells and interference-expressed SH-SY5Y cells. Gene Ontology functional enrichment analysis showed that these DEGs played significant roles in the growth, development, and regeneration of axons, DNA biosynthetic processes, DNA replication, and apoptosis. Kyoto Encyclopedia of Genes and Genomes enrichment analysis indicated that these DEGs were found in some pathways, including ferroptosis, glutamatergic synapses, protein processing in the endoplasmic reticulum, estrogen signaling pathways, the TGF-beta signaling pathway, and the longevity regulating pathway. The qRT-PCR validation results were consistent with RNA-seq results, which showed that HSPA5, IGFBP3, NTN4, and KLF9 increased in ZNF580-overexpressed SH-SY5Y cells and decreased in interference-expressed SH-SY5Y cells, when compared with normal cells. Together, the results suggested that ZNF580 targeted these genes to inhibit neuronal apoptosis.

Asunto(s)

RESUMEN

This study was designed to investigate the effects of astragalosides on cardiac diastolic function, and an emphasis was placed on the variation of the upstream molecular regulators of phospholamban. Chronic heart failure (CHF) rats were induced by ligaturing the left anterior coronary artery, and rats in the therapeutic groups were treated with either a 50 mg/kg dose of captopril, 10 mg/kg dose of astragalosides or 20 mg/kg dose of astragalosides. Four weeks after treatment, the ratio of the early and atrial peak filling velocities (E/A) and maximal slope diastolic pressure decrement (-dp/dt) both decreased in CHF rats (by 30.3% and 25.5%, respectively) and significantly increased in 20 mg/kg astragalosides and captopril-treated rats. The protein phosphatase-1 activity was lower in the 20 mg/kg astragalosides group than in the CHF group (0.22 vs 0.44, P < 0.01), and the inhibitor-1 levels in the astragalosides and captopril-treated groups were increased. Chronic heart failure increased expression of protein kinase C-α and calcium-sensing receptor, and these changes were attenuated by astragalosides therapy. Astragalosides restored the diastolic dysfunction of chronic heart failure rats, possibly by downregulation of calcium-sensing receptor and protein kinase C-α, which in turn augmented inhibitor-1 expression, reduced protein phosphatase-1 activity and increased phospholamban phosphorylation.

Asunto(s)

RESUMEN

OBJECTIVE: To investigate the effects of the Traditional Chinese Medicine berberine on blood lipid and antioxidation ability in hyperlipoidemic model rats. METHODS: Ten rats were randomly chosen as control group, and other rats were used to establish hyperllipemia rat models. Successfully molding rats were randomly divided into model group, berberine low dose group(100 mg/kg), medium dose group(200 mg/kg), high dose group(300 mg/kg), and xuezhikang group(200 mg/kg), 10 rats in each group. Each rat received gavage per day continually for 30 days. Diacylgycerol acyltransferase (DGAT), 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA), hepatic triglycerides lipase (HTGL), cholesterol 7a-hydroxylase (CYP7A), triglyceride (TG), total cholesterol (TC), low density lipoprotein (LDL), high-density lipoprotein (HDL), malondialdehyde (MDA), glutathion peroxidase (GSH-Px) and superoxide dismutase (SOD) levels were monitored. RESULTS: The Traditional Chinese Medicine berberine could obviously decrease the liver coefficient and the contents of TC, TG, LDL-C and increase the serum content of HDL-C in hyperlipoidemia rats. The Traditional Chinese Medicine berberine decrease the levels of MDA, DGAT, HMG-CoA and increase the activities of HTGL, CYP7A, SOD and GSH-Px in liver tissue. CONCLUSIONS: The Traditional Chinese Medicine berberine could decrease the blood lipid level and prevent the lipid peroxidation damage in hyperlidemia rats.

Asunto(s)

RESUMEN

The study investigated the beneficial effects of astragalosides (AS) on cardiac performance in rats with chronic heart failure. Chronic heart failure was produced by left anterior descending coronary artery ligation, and the therapeutic efficacy of astragalosides at 10, 20 and 40 mg/kg was evaluated. Five weeks after the operation, cardiac function was deficient and sarcoplasmic reticulum Ca²âº-ATPase (SERCA) activity was significantly reduced. Moreover, SERCA mRNA decreased, while expression of the SERCA down-regulator phospholamban (PLB) was significantly increased. Phosphorylated phospholamban (P-PLB), the form that does not inhibit SERCA, was also reduced by chronic heart failure. Treatment with AS improved left ventricle function and cardiac structure, reversed the depression of SERCA activity, and increased P-PLB. These results suggest that the cardioprotective effect of AS may be due to the increase in P-PLB protein, which disinhibits SERCA activity. Rescue of sarcoplasmic reticulum Ca²âº cycling by astragalosides could normalize excitation-contraction coupling and improve overall cardiac function.

Asunto(s)