ELK1270 Human IL1b (Interleukin 1 Beta) ELISA Kit

Icariin (ICA), a flavonol glycoside isolated from Epimedium, has been considered as a potential alternative therapy for ischemic stroke. However, the protective mechanisms of ICA on cerebral ischemia-reperfusion (I/R) are not fully illuminated yet. The effects of ICA on ER stress and inflammatory response which were involved in the pathological process of cerebral I/R were investigated in vitro. Microglia and neurons were subjected to OGD/R. ICA was administrated to microglia 1 h before OGD and maintained 2 h throughout OGD. At 24 h after reoxygenation, the protein expression of IL-1 β, IL-6, TNF-α in the supernatant of microglia was measured using ELISA assay; neuronal apoptosis was assessed by TUNEL staining; and cell viability was detected using CKK-8 assay; the expression of IRE1α, XBP1u, XBP1s, and cleaved caspase-3 in neurons was examined by western blotting and qRT-PCR; the expression of p-IRE1α in neurons was detected by western blotting. We found that OGD/R induced the expression of IL-1 β, IL-6, TNF-α in the supernatant of microglia; OGD/R and these proinflammatory cytokines promoted the mRNA as well as protein expression of XBP1u, XBP1s and cleaved caspase-3, increased the ratio of p-IRE1α/IRE1α, as well as apoptosis, and decreased cell viability in primary cortical neurons, while ICA reversed the levels of the above factors. IRE1 overexpression enhanced ER stress as well as apoptosis, and impaired the protective effects of ICA. These results suggested that ICA can inhibit apoptosis in neurons after OGD/R through IRE1/XBP1 signaling pathway beside its anti-inflammatory effect.

c-jun N-terminal kinase (JNK) plays pivotal roles in many physiological processes, including inflammation and glucose metabolism. However, the effects of JNK on olanzapine-induced insulin resistance and the underlying mechanisms have not been fully elucidated. The aim of our study was to explore the role of JNK in olanzapine-induced insulin resistance and the underlying mechanisms.

Background Cissus quadrangularis L. is commonly known as hadjod and traditionally used as a medicinal plant for the treatment of osteoporosis, dyspepsia, tumors, chronic ulcers, and hepatic diseases. Existing studies have proclaimed the proinflammatory property of NOX4 through instigating ROS and oxidative stress, which is considered to be one of the instrumental causes of steatohepatitis. Purpose To investigate the protective effect of ethanolic extract of C. quadrangularis (EECQ) on the steatohepatitis associated with type 2 diabetes (DM) through inhibition of NOX4. Methods An experimental DM-induced steatohepatitis was developed by feeding a high-fat diet for 12 weeks in Sprague Dawley rats. Treatment of EECQ was given at a dose of 200 mg/kg (po), for six weeks. Glucose and insulin tolerance test was conducted. Hematoxylin and eosin and picrosirius red staining of liver sections was done. Steatosis and lobular inflammation were scored, and hepatocyte ballooning was assessed to confirm the NASH. qPCR, Immunofluorescence, and Immunoblotting determined the mRNA and protein expression of NOX4. Results NASH group rats manifested features of DM, marked by aggravated glucose and insulin tolerance tests. Moreover, the DM rats exhibited the presence of steatohepatitis, characterized by elevated serum lipid content, aminotransferases, and presence of steatosis, lobular inflammation, and ballooning in the liver section. Nevertheless, EECQ treatment prevented all of these abnormalities. Besides, the level of AGEs and the expression of its receptor, RAGE was found to be increased in DM rats. Parallelly, the expression of NOX4 and the accompanying level of ROS, oxidative stress markers, and inflammatory cytokines were determined to be surged in palmitic acid exposed HepG2 cells and DM rats. However, EECQ treatment exemplified safeguards from the soared level of the aforementioned markers. Conclusion Collectively, the above findings propounded the protective effect of EECQ against steatohepatitis. Nonetheless, further studies on humans necessitate to scrutinize and reinforce its therapeutic potential so that it may be employed as a remedy for DM-induced steatohepatitis.

Despite improvements in antimicrobial therapy and supportive care, sepsis is still a major public health issue. Recently, CD100 and its receptor in the immune system CD72 were shown to play a major role in immune regulation. The purpose of this study was to investigate the expression and clinical correlations of CD72 and CD100 on circulating lymphocytes of septic 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.

Previous study disclosed Fucosyltransferase 2 (Fut2) gene as a IBD risk locus. This study aimed to explore the mechanism of Fut2 in IBD susceptibility and to propose a new strategy for the treatment of IBD.

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.