Rotavirus enteritis (RVE) is a common acute intestinal infectious disease caused by rotavirus infection. It is an important cause of death in children younger than 5 years worldwide. Shenling baizhu powder (SBP), a classic traditional Chinese formulation, is one of the most popularly prescribed medicines for digestive diseases. Clinical studies have revealed the protective effects of SBP on RVE. However, the potential mechanism is still unclear. In this study, we aimed to evaluate the anti-rotavirus effect of SBP and its mechanism, focusing on the TLR4/MyD88/NF-κB signaling pathway. Our results demonstrated that, based on the inhibition of the virus-induced cytopathic effect in Caco-2 cells, the concentration for 50% of maximal effect (EC50) and selectivity index (SI) of SBP for RV-SA11 in the serum were 5.911% and 11.63, respectively. A total of 219 active compounds with oral bioavailability ≥30% and drug-likeness ≥ 0.18 were selected from the 10 ingredients present in the formulation of SBP, which acted on 471 potential targets. A total of 226 target genes of RVE were obtained from the GeneCards database. The protein-protein interaction (PPI) network showed that there was a close interaction between 44 common targets of SBP and RVE. The results of Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis showed that SBP acted on RVE through various inflammatory pathways and the intestinal immune network. Subsequently, we investigated the effect of SBP on TLR4/MyD88/NF-κB signaling pathway in vitro. After infection with RV- SA11, the expression of TLR4, MyD88, and NF-κB mRNA and protein increased significantly, which could be abolished by SBP treatment. In addition, the IL-1β, TNF-α, IL-6, and IFN-β levels increased markedly in Caco-2 cells infected with RV-SV11. Treatment with SBP partly reversed the changes of IL-1β, TNF-α, and IL-6, while further increased the level of IFN-β. In conclusion, our study revealed that SBP can significantly inhibit rotavirus replication and proliferation in vitro. The antiviral effect may be related to the regulation of the TLR4/MyD88/NF-κB signaling pathway, followed by the down regulation of inflammatory cytokines and up regulation of IFN-β induced by rotavirus.

The therapeutic effect of sacubitril/valsartan (S/V) on heart failure has been confirmed, while its role in atherosclerosis remains largely unexplored. The present study aimed to investigate the effects of S/V on the expression of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), inflammation and apoptosis in human umbilical vein endothelial cells (HUVECs) induced by oxidized low-density lipoprotein (ox-LDL) and to elucidate its possible mechanism. Cell Counting Kit-8 assay was used to detect cell viability. Reverse transcription-quantitative PCR was performed to detect the MALAT1 expression. ELISA was performed to detect the levels of IL-1β, IL-6 and TNF-α. Flow cytometry was conducted to detect the apoptotic rate of cells. A nitric oxide (NO) detection kit was used to determine the concentration of NO. Western blotting analysis was performed to determine the levels of intercellular cell adhesion molecule (ICAM)-1, vascular cell adhesion molecule (VCAM)-1, endothelin-1, caspase-3, Bax, Bcl-2, Toll-like receptor 4 (TLR4), p65 and p-p65. Compared with the ox-LDL group, S/V treatment significantly increased the cell viability, NO concentration and Bcl-2 expression, decreased the levels of IL-1β, IL-6 and TNF-α and reduced the expressions of MALAT1, ICAM-1, VCAM-1, cleaved-caspase-3, Bax, TLR4 and p-p65. Overall, the findings suggested that S/V could downregulate the expression of MALAT1, inhibit inflammation and apoptosis and improve endothelial function in ox-LDL-induced HUVECs via inactivating the TLR4/NF-κB signaling pathway. Therefore, S/V might be utilized as a promising therapeutic strategy for the prevention and treatment of atherosclerosis.

Background. Ulcerative colitis (UC) is a kind of inflammatory bowel disease which is needed to be predicted. Objective. To analyze various animal models of UC conditions and summarizes the animal selection, model progression, and pathogenic mechanisms of UC animal models. Methods. We surveyed the research papers published in PubMed, Google Scholar, Baidu Scholar, CNKI, SciFinder, and Web of Science in the past 5 years and discussed the experimental animals, modeling methods, and pathogenic mechanisms. Results. In the selection of experimental animals, rats are considered the best experimental animals. The mainstream modeling methods can be categorized into the chemical stimulation method, immune stimulation method, and compound method, among which the compound method is the most successful. In the study of the pathogenesis of UC, the pathogenesis of UC is due to various pathogenic factors, such as nitric oxide (NO), prostaglandins (PG), proinflammatory factors (IL, TNF-α), and intestinal flora. Conclusion. The method of building an animal model of UC is well-established, providing a more targeted selection of animal models for future related experiments.

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Flowers are generally short-lived, and they all face a multidimensional challenge because they have to attract mutualists, compel them to vector pollen with minimal investment in rewards, and repel floral enemies during this short time window. Their displays are under complex selection, either consistent or conflicting, to maximize reproductive fitness under heterogeneous environments. The phenological or morphological mismatches between flowers and visitors will influence interspecific competition, resource access, mating success and, ultimately, population and community dynamics. To better understand the effects of the plant visitors on floral traits, it is necessary to determine the functional significance of specific floral traits for the visitors; how plants respond to both mutualists and antagonists through adaptive changes; and to evaluate the net fitness effects of biological mutualisms and antagonism on plants. In this review, we bring together insights from fields as diverse as floral biology, insect behavioral responses, and evolutionary biology to explain the processes and patterns of floral diversity evolution. Then, we discuss the ecological significance of plant responses to mutualists and antagonists from a community perspective, and propose a set of research questions that can guide the research field to integrate studies of plant defense and reproduction.