Histopathological analysis of the joint tissue confirmed the reduction of inflammatory signs. In the ethanol-induced gastric ulcer model, free nerolidol reduced the relative ulcer area more expressively (4.64%) than the inclusion complex (21.3%). However, in the indomethacin induction model, the inclusion complex showed better results in gastric protection compared to free nerolidol. The action of nerolidol complexed in beta-cyclodextrin in reducing arthritis inflammation combined with its gastroprotective action make it a potential new drug.

Alterations in the respiratory and digestive tract microbiomes influence the occurrence and progression of chronic obstructive pulmonary disease (COPD). Here, we aimed to identify fecal microbiome profiles during COPD development.

Fecal samples were collected from 29 COPD patients with acute exacerbation (AECOPD), 29 stable COPD patients, and 22 normal subjects (NS). The fecal microbial profiles were obtained using 16S rRNA gene sequencing.

The diversity and richness were lower and fewer variations in the taxonomic composition of fecal microbiota were observed in AECOPD patients than in stable COPD and NS. The relative abundances of Firmicutes and Actinobacteria were decreased, while those of Bacteroidetes and Proteobacteria were increased in AECOPD compared to COPD and NS. Among the top ten genera, the proportions of Lachnoclostridium and Parabacteroides significantly increased in AECOPD, whereas those of other genera decreased. Discriminative bacteria, such as p_Bacteroidetes, c_Bacteroidia, o_Bacteroidales, Lactobacillales, and Proteobacteria, were identified in AECOPD compared to stable COPD and NS. The weighted gene co-expression networks showed that Firmicutes and Actinobacteria were the main hub bacterial taxa related with lung function (FEV1% and FEV1/FVC%) and inflammatory indices (TNF-α, IL-6, IL-8, PCT, and CRP).

These findings emphasized the changes in the abundance and composition of the fecal microbiome in stable COPD and AECOPD. Variations in fecal microbiota may be associated with COPD progression.

These findings emphasized the changes in the abundance and composition of the fecal microbiome in stable COPD and AECOPD. Variations in fecal microbiota may be associated with COPD progression.Breast cancer is one of the most malignant diseases world-wide and ranks the first among female cancers. Progranulin (PGRN) plays a carcinogenic role in breast cancer, but its mechanisms are not clear. In addition, there are few reports on the relationship between PGRN and tumor-associated macrophages (TAMs).

To investigate the effects of exosomes derived from PGRN

TAMs on invasion and migration of breast cancer cells.

Mouse breast cancer xenograft model was constructed to explore the effect of PGRN

tumor environment (TME) on breast cancer. Flow cytometry was used to compare TAMs of wild type (WT) and PGRN

tumor tissue. Transwell assay, wound healing assay and western blot were used to explore the effect of WT and PGRN

TAMs and their exosomes on invasion, migration and epithelial-mesenchymal transition (EMT) of breast cancer cells. MicroRNA (miRNA) assay was used to find out the differentially expressed miRNA of negative control (NC) and siPGRN-TAMs exosomes. Quantitative PCR and luciferase report assay were used to explore the target gene.

The lung metastasis of breast cancer of PGRN

mice was inhibited. PGRN

TAMs inhibited invasion, migration and EMT of breast cancer cells through their exosomes. MiR-5100 of PGRN

TAMs-derived exosomes was up-regulated, which might regulate expression of CXCL12, thereby inhibiting the CXCL12/CXCR4 axis, and ultimately inhibiting the invasion, migration and EMT of breast cancer cells.

Our study elucidates a new molecular mechanism of lung metastasis of breast cancer, so it may contribute to efficient prevention and therapeutic strategies.

Our study elucidates a new molecular mechanism of lung metastasis of breast cancer, so it may contribute to efficient prevention and therapeutic strategies.

Autophagy has been reported to play an essential role in fibrotic disorders. Known as fibrotic cataract, posterior capsular opacification (PCO) result from pathological epithelial-mesenchymal transition (EMT) of lens epithelial cells (LECs). This study aims to identify the role and potential mechanism of autophagy in TGF-β2-induced EMT in LECs.

Primary rabbit LECs were treated with TGF-β2 to induce EMT as a model of fibrotic cataract in vitro. 3-methyladenine, chloroquine, bafilomycin A1, and gene silencing of autophagy-related protein 7 (ATG7) were treated in LECs for autophagy inhibition, while rapamycin was utilized for autophagy activation. The expression levels of EMT/autophagy-associated markers were analyzed by qRT-PCR, western blotting, immunofluorescence and transmission electron microscopy. We additionally examined cell migration ability with transwell migration assay and wound healing assay.

TGF-β2 promoted autophagy flux during EMT progression of LECs in a time-dependent manner. Autophagy activation by rapamycin enhanced TGF-β2-triggered fibrogenic responses and cell migration in LECs, whereas pharmacological inhibition of autophagy alleviated TGF-β2-induced increases of EMT markers and cell migration of LECs. In addition, the phosphorylation of Smad2/3 induced by TGF-β2 was suppressed through autophagy inhibition, while it was promoted upon autophagy activation, indicating that TGF-β2/Smad signaling was involved in the modulation of autophagy on EMT in LECs. Furthermore, ATG7-silenced LECs exerted anti-fibrosis effect induced by TGF-β2 through downregulation of autophagy.

Intervention/inhibition of autophagy could attenuate TGF-β2-induced EMT in LECs, which provides autophagy-related insights on preventing and treating the fibrotic cataract or other fibrotic diseases.

Intervention/inhibition of autophagy could attenuate TGF-β2-induced EMT in LECs, which provides autophagy-related insights on preventing and treating the fibrotic cataract or other fibrotic diseases.

Sepsis is a systemic inflammatory complication, which is the common cause of death in critical patients. This study aimed to evaluate the potential regulatory mechanisms of miR-150 in lipopolysaccharide (LPS)-challenged HUVECs and cecal ligation and puncture (CLP)-induced septic mice.

Human umbilical vein endothelial cells (HUVECs) were challenged with LPS. Pulmonary arterial endothelial cells (PAECs) were isolated from CLP-induced septic mice. CMC-Na in vivo The mRNA and protein levels of target molecules were detected by RT-qPCR and Western blotting. Apoptosis of HUVECs was determined by Annexin V/PI staining on a flow cytometry. The interaction between miR-150 and MALAT1 was assessed by luciferase reporter assay, RIP and RNA pull-down assay.

MiR-150 was downregulated in LPS-induced HUVECs. MiR-150 mimics restrained LPS-induced inflammatory response by reducing TNF-α and IL-6 levels, but increasing IL-10 level. Moreover, miR-150 mimics downregulated endoplasmic reticulum (ER) stress-related proteins, GRP78 and CHOP levels in LPS-exposed HUVECs.