ELK1142 Human IL10 (Interleukin 10) ELISA Kit

Despite significant advances in the diagnosis and management of sepsis and trauma over the past few decades, severe infection and injury continue to represent major public health challenges. Fibrinogen-like protein 2 (FGL2), a member of the fibrinogen family, can be expressed as a membrane-associated protein with coagulation activity or in a secreted form possessing unique immune suppressive functions. In this study, we evaluated whether soluble fibrinogen-like protein 2 (sFGL2) can serve as a biomarker to predict the development of sepsis in trauma patients.

Non-small cell lung cancer (NSCLC) is the most common malignant tumor of lung, which seriously threatens the life of people. It has been reported that lncRNA prostate cancer-associated transcript 6 (PCAT6) could facilitate the metastasis of NSCLC cells. However, whether lncRNA PCAT6 in NSCLC cells could affect the tumor microenvironment (TME) remains unclear. In the present study, the level of PCAT6 in NSCLC cells was detected using RT-qPCR. The effects of PCAT6 knockdown on the viability and apoptosis in NSCLC cells were detected with CCK-8 and flow cytometry assay. NSCLC cell-derived exosomes were isolated with ultracentrifugation. Next, transwell assay was conducted to assess the migration and invasion of NSCLC cells. Dual-luciferase reporter assay was performed to verify the relationship among PCAT6, miR-326, and KLF1 in A549 cells. In addition, nanoparticle tracking analysis (NTA) was applied to detect the particle size of isolated exosomes. Moreover, ELISA assay was performed to detect the levels of IL-1β and IL-10 in the supernatant of macrophage. We found knockdown of PCAT6 significantly inhibited the viability, migration, and invasion of NSCLC cells. In addition, dual-luciferase reporter assay illustrated that miR-326 was the target of PCAT6 and KLF1 was the target of miR-326 in NSCLC cells. Moreover, NSCLC cells-derived exosomes could promote macrophages M2 polarization by transporting PCAT6. Meanwhile, macrophages M2 polarization was able to promote the metastasis and epithelial-mesenchymal transition (EMT) process of NSCLC cells via regulating PCAT6/miR-326/KLF1 axis. Taken together, knockdown of lncRNA PCAT6 suppressed the growth of NSCLC cells by inhibiting macrophages M2 polarization via miR-326/KLF1 axis.

Endometritis seriously affects women’s normal life and work. It has been found that microRNA-123-3p (miR-124-3p) expression is abnormally high expression in the patients of chronic endometritis. However, the underlying mechanism for miR-124-3p regulation of endometritis development remains unclear. In our study, we treated human endometrial epithelial cells (HEECs) with LPS to simulate endometrial injury in vitro. Then, HEEC was treated with miR-124-3p mimics and miR-124-3p inhibitor. Next, exosomes were separated from bone marrow-derived mesenchymal stem cells (BMSCs). In addition, BMSCs were co-cultured with HEEC. Later on, dual-luciferase reporter assay was carried out to validate the regulation between miR-124-3p and DUSP6. Results indicated that LPS inhibited the viability of HEEC in time and dose dependent manner. MiR-124-3p inhibitor reversed apoptosis and viability inhibition of HEEC which were induced by LPS. In addition, we also found exosomes could transfer miR-124-3p from BMSCs to HEEC. Besides, BMSCs/anti-miR-124-3p Exo was observed to abolish LPS-induced viability and proliferation inhibition of HEEC by inducing the apoptosis of HEEC. Moreover, BMSCs/anti-miR-124-3p Exo alleviated inflammation of HEEC induced by LPS via upregulating DUSP6 and downregulating p-p65 and p-ERK. Furthermore, BMSCs/anti-miR-124-3p Exo protected against LPS-induced endometritis in vivo by upregulating DUSP6 and downregulating p-p65 and p-ERK. In conclusion, we found that BMSCs/anti-miR-124-3p Exo might be a promising new alternative to treat endometritis.

Gallbladder cancer (GBC) ranks seventh among the gastrointestinal cancers. Messenger RNAs (mRNAs) could regulate the progression of GBC. For the purpose of exploring the targets for GBC treatment, RNA sequencing was used to identify the differential expressed mRNAs between GBC and adjacent tissues. Next, CCK8 assay was used to assess the cell viability, and cell proliferation was investigated by colony formation assay. Flow cytometry was performed to evaluate the cell apoptosis. Protein and mRNA expression were analyzed by western blot and RT-qPCR, respectively. Transwell was performed to evaluate the cell metastasis. GBC-derived exosomes were isolated with ultracentrifugation. To evaluate the function of exosomes in GBC, in vivo model of GBC was constructed. The data revealed IGF2BP3 was identified to be upregulated in GBC, and IGF2BP3 silencing was able to decrease GBC cell proliferation by promoting the apoptosis. The migration and invasion of GBC cells were reduced by IGF2BP3 knockdown. Silencing of IGF2BP3 obviously suppressed the level of p-STAT3 in GBC cells. Meanwhile, GBC cell-derived exosomes notably promoted macrophage M2 polarization via carrying IGF2BP3, and then the polarized macrophages promoted the malignant behavior of GBC cells. Furthermore, exosomes markedly promoted the tumor growth of GBC via promoting macrophage M2 polarization. In summary, knockdown of IGF2BP3 suppressed the malignant behavior of GBC cells. Additionally, knockdown of IGF2BP3 modified tumor microenvironment during the progression of GBC. Thus, these findings might provide a new theoretical basis for exploring a strategies against GBC.