Inflammation is a complex physiological process that poses a serious threat to people's health. However, the potential molecular mechanisms of inflammation are still not clear. Moreover, there is ...lack of effective anti-inflammatory drugs that meet the clinical requirement. Procyanidin A1 (PCA1) is a monomer component isolated from Procyanidin and shows various pharmacological activities. This study further demonstrated the regulatory role of PCA1 on lipopolysaccharide (LPS)-stimulated inflammatory response and oxidative stress in RAW264.7 cells. Our data showed that PCA1 dramatically attenuated the production of pro-inflammatory cytokines such as NO, iNOS, IL-6, and TNF-α in RAW264.7 cells administrated with LPS. PCA1 blocked IκB-α degradation, inhibited IKKα/β and IκBα phosphorylation, and suppressed nuclear translocation of p65 in RAW264.7 cells induced by LPS. PCA1 also suppressed the phosphorylation of JNK1/2, p38, and ERK1/2 in LPS-stimulated RAW264.7 cells. In addition, PCA1 increased the expression of HO-1, reduced the expression of Keap1, and promoted Nrf2 into the nuclear in LPS-stimulated RAW264.7 cells. Cellular thermal shift assay indicated that PCA1 bond to TLR4. Meanwhile, PCA1 inhibited the production of intracellular ROS and alleviated the depletion of mitochondrial membrane potential in vitro. Collectively, our data indicated that PCA1 exhibited a significant anti-inflammatory effect, suggesting that it is a potential agent for the treatment of inflammatory diseases.
Adaptive evolution following colonization can affect the impact of invasive species. The fall webworm (FWW) invaded China 40 years ago through a single introduction event involving a severe ...bottleneck and subsequently diverged into two genetic groups. The well‐recorded invasion history of FWW, coupled with a clear pattern of genetic divergence, provides an opportunity to investigate whether there is any sign of adaptive evolution following the invasion. Based on genome‐wide SNPs, we identified genetically separated western and eastern groups of FWW and correlated spatial variation in SNPs with geographical and climatic factors. Geographical factors explained a similar proportion of the genetic variation across all populations compared with climatic factors. However, when the two population groups were analysed separately, environmental factors explained more variation than geographical factors. SNP outliers in populations of the western group had relatively stronger response to precipitation than temperature‐related variables. Functional annotation of SNP outliers identified genes associated with insect cuticle protein potentially related to desiccation adaptation in the western group and genes associated with lipase biosynthesis potentially related to temperature adaptation in the eastern group. Our study suggests that invasive species may maintain the evolutionary potential to adapt to heterogeneous environments despite a single invasion event. The molecular data suggest that quantitative trait comparisons across environments would be worthwhile.
During their lifetime, plants encounter numerous biotic and abiotic stresses with diverse modes of attack. Phytohormones, including salicylic acid (SA), ethylene (ET), jasmonate (JA), abscisic acid ...(ABA), auxin (AUX), brassinosteroid (BR), gibberellic acid (GA), cytokinin (CK) and the recently identified strigolactones (SLs), orchestrate effective defense responses by activating defense gene expression. Genetic analysis of the model plant
has advanced our understanding of the function of these hormones. The SA- and ET/JA-mediated signaling pathways were thought to be the backbone of plant immune responses against biotic invaders, whereas ABA, auxin, BR, GA, CK and SL were considered to be involved in the plant immune response through modulating the SA-ET/JA signaling pathways. In general, the SA-mediated defense response plays a central role in local and systemic-acquired resistance (SAR) against biotrophic pathogens, such as Pseudomonas syringae, which colonize between the host cells by producing nutrient-absorbing structures while keeping the host alive. The ET/JA-mediated response contributes to the defense against necrotrophic pathogens, such as
, which invade and kill hosts to extract their nutrients. Increasing evidence indicates that the SA- and ET/JA-mediated defense response pathways are mutually antagonistic.
Lithium (Li) metal is a promising anode material for high‐energy density batteries. However, the unstable and static solid electrolyte interphase (SEI) can be destroyed by the dynamic Li ...plating/stripping behavior on the Li anode surface, leading to side reactions and Li dendrites growth. Herein, we design a smart Li polyacrylic acid (LiPAA) SEI layer high elasticity to address the dynamic Li plating/stripping processes by self‐adapting interface regulation, which is demonstrated by in situ AFM. With the high binding ability and excellent stability of the LiPAA polymer, the smart SEI can significantly reduce the side reactions and improve battery safety markedly. Stable cycling of 700 h is achieved in the LiPAA‐Li/LiPAA‐Li symmetrical cell. The innovative strategy of self‐adapting SEI design is broadly applicable, providing opportunities for use in Li metal anodes
Stretching exercises: A flexible lithium polyacrylic acid (LiPAA) solid electrolyte interphase (SEI) layer which is highly stretchable is designed to address the dynamic volume changes during Li plating/stripping on the Li anode surface in Li ion batteries. The LiPAA polymer SEI can significantly reduce the side reactions and improve the safety performance.
Glycogen synthase kinase‐3 (GSK3) is a highly evolutionarily conserved serine/threonine protein kinase first identified as an enzyme that regulates glycogen synthase (GS) in response to insulin ...stimulation, which involves GSK3 regulation of glucose metabolism and energy homeostasis. Both isoforms of GSK3, GSK3α, and GSK3β, have been implicated in many biological and pathophysiological processes. The various functions of GSK3 are indicated by its widespread distribution in multiple cell types and tissues. The studies of GSK3 activity using animal models and the observed effects of GSK3‐specific inhibitors provide more insights into the roles of GSK3 in regulating energy metabolism and homeostasis. The cross‐talk between GSK3 and some important energy regulators and sensors and the regulation of GSK3 in mitochondrial activity and component function further highlight the molecular mechanisms in which GSK3 is involved to regulate the metabolic activity, beyond its classical regulatory effect on GS. In this review, we summarize the specific roles of GSK3 in energy metabolism regulation in tissues that are tightly associated with energy metabolism and the functions of GSK3 in the development of metabolic disorders. We also address the impacts of GSK3 on the regulation of mitochondrial function, activity and associated metabolic regulation. The application of GSK3 inhibitors in clinical tests will be highlighted too. Interactions between GSK3 and important energy regulators and GSK3‐mediated responses to different stresses that are related to metabolism are described to provide a brief overview of previously less‐appreciated biological functions of GSK3 in energy metabolism and associated diseases through its regulation of GS and other functions.
Breast cancer is a kind of common female cancers. Increasing evidence has exhibited that lncRNAs exert a crucial role in breast cancer. So far, the mechanism of lncRNAs in breast cancer is still not ...well established. In our current study, we focused on the biological role of lncRNA Nuclear Enriched Abundant Transcript 1 (NEAT1) in breast cancer. We observed that NEAT1 levels were significantly increased in human breast cancer cells including MCF‐7, MDA‐MB‐453, MDA‐MB‐231, and SKBR3 cells compared to normal mammary epithelial cells MCF‐10A while miR‐448 was decreased. We found that downregulation of NEAT1 was able to inhibit the growth of breast cancer cells and miR‐448 mimic exerted the similar function. Bioinformatics analysis and dual luciferase reporter assays confirmed the negative correlation between NEAT1 and miR‐448 in vitro. In addition, ZEB1 was predicted as a novel mRNA target of miR‐448. Overexpression of NEAT1 can induce breast cancer cell growth, migration, and invasion by inhibiting miR‐448 and upregulating ZEB1. It was demonstrated that NEAT1 can increase ZEB1 levels while miR‐448 mimic can repress ZEB1. It was speculated in our study that NEAT1 can serve as a competing endogenous lncRNA (ceRNA) to modulate ZEB1 by sponging miR‐448 in breast cancer. To conclude, we uncovered that NEAT1 participated in breast cancer progression by regulating miR‐448 and ZEB1. NEAT1 can be provided as a vital biomarker in breast cancer diagnosis and treatment therapy.
Our results implied that NEAT1 can play a significant role in breast cancer progression. We observed that NEAT1 downregulation could inhibit breast cancer progression. In addition, a reverse correlation between NEAT1 and miR‐448 was validated in our research, and ZEB1was concentrated on in our investigation asit can be targeted by miR‐448.
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