ABSTRACT
Objective:To investigate the effect of Huayu Jiedu prescription medicated serum（HJRMS）on the proliferation， invasion and migration of human lung cancer cells （H1299 cells） and its mechanism. Method:Cell counting kit-8 （CCK-8） method was used to detect the inhibitory effect of HJRMS on the proliferation of lung cancer cells， the effect of HJRMS on the invasion and migration of H1299 cells were determined by Transwell assay and wound healing assay. The protein expressions of Janus kinase 2 （JAK2）， signal transduction and activation transcription factor 3 （STAT3）， phosphorylated JAK2（p-JAK2） and phosphorylated STAT3 （p-STAT3） were detected by Western blot， the mRNA expression levels of JAK2 and STAT3 were detected by Real-time quantitative polymerase chain reaction（Real-time PCR）. Result:① Compared with control group， the proliferation of H1299 cells was significantly inhibited after treatment with 1%~16%HJRMS serum for 24， 48 h， respectively（<italic>P</italic><0.01）， and showed a certain concentration dependence. ② After treatment with HJRMS for 24 h， the scratch healing ability of cells in the 4%，8%HJRMS serum groups was inhibited（<italic>P</italic><0.05，<italic>P</italic><0.01）. ③ Compared with control group， the membrane permeability of H1299 cells in invasion and migration experiments in 2%，4%，8%HJRMS serum groups was decreased significantly（<italic>P</italic><0.05，<italic>P</italic><0.01）. ④ Western blot showed that compared with control group， 4%，8%HJRMS serum groups inhibited the expression of JAK2/STAT3 signaling pathway related proteins （JAK2， p-JAK2， STAT3， and p-STAT3） in lung cancer H1299 cells（<italic>P</italic><0.05， <italic>P</italic><0.01）. ⑤ Compared with control group， the mRNA expression levels of JAK2 and STAT3 in lung cancer H1299 cells treated with 8%HJRMS for 24 h decreased significantly （<italic>P</italic><0.05）. Conclusion:The HJRMS can inhibit the proliferation， invasion and migration of lung cancer H1299 cells， and its mechanism may be related to the inhibition of JAK2/STAT3 signaling pathway.
ABSTRACT
Objective:To observe the effect of Huayu Jiedu recipe （HYJDR） on apoptosis of gastric cancer cells， explore the mechanism of HYJDR on apoptosis of gastric cancer cells and provide experimental basis for clinical application of HYJDR. Method:Thiazolyl blue tetrazolium bromide （MTT） method was used to detect the effect of HYJDR （5，10，15，20，25，30 g·L-1） on the activity of SGC-7901 cells and the median inhibition concentration （IC50） of HYJDR on SGC-7901 cells. Propidium iodide （PI） and Hoechst double fluorescence staining were used to detect the effect of HYJDR on the apoptosis of gastric cancer SGC-7901 cells. Western blot was used to detect the effect of HYJDR on the expression of apoptosis related proteins in gastric cancer cells. Real-time polymerase chain reaction （Real-time PCR） was used to detect the effect of HYJDR on the expression of apoptosis related protein mRNA in gastric cancer cells. Result:As compared with blank group， HYJDR （>10 g·L-1） can significantly inhibit the proliferation of gastric cancer cells. With the increase of the concentration of HYJDR， the cell viability decreased significantly obviously in a concentration-dependent manner（P<0.05）. HYJDR can significantly promote the apoptosis of gastric cancer cells. With the increase of the concentration of HYJDR， the apoptosis of gastric cancer cells gradually increased. As compared with blank group， HYJDR can obviously inhibit the expression of apoptosis-related B -cell lymphoma-2 （Bcl-2） （P<0.05）， and increase the expression of apoptosis-promoting proteins such as Bcl-2 antagonist of cell death （Bad） and Bcl-2-associated X （Bax）（P<0.05）. Real-time PCR results showed that as compared with blank group， HYJDR（5，10 g·L-1） could effectively inhibit the expression of Bcl-2 protein mRNA in gastric cancer cells（P<0.05）， and all HYJDR groups could promote the expression level of Bad mRNA（P<0.05）. Conclusions:HYJDR can obviously promote the apoptosis of SGC-7901， and its effect is probably achieved by increasing the expression of Bad mRNA and inhibiting the expression of Bcl-2 protein.
ABSTRACT
OBJECTIVE@#To investigate the effect of IL-27 on Th17 cells in patients with henoch-schönlein purpura（HSP） in order to further elucidate the pathogenesis.@*METHODS@#Fifty patients with HSP treated in our hospital from April 2019 to July 2019 were selected as HSP group, and 30 volunteers underwent physical examination at the same time were selected as control group. The proportion of Th17 cells in peripheral blood of HSP group and healthy control group was determined by flow cytometry (FCM). A total of 27 HSP patients were selected, and candidate peripheral blood mononuclear lymphocytes (PBMC) were co-cultured with exogenous rhIL-27, and the ratio of Th17 cells was detected by flow cytometry.@*RESULTS@#The proportion of Th17 cells in the peripheral blood of HSP patients with acute phase was (1.57±0.54)%, which was significantly higher than that of the control group (0.86±0.40)% (t=-6.298, P<0.001), and the proportion of Th17 cells was decreased significantly after rhIL-27 co-culture (1.39%±0.52% vs 0.98%±0.44%)(P<0.05).@*CONCLUSION@#IL-27 can reduce the level of Th17 cells in patients with HSP, which may be involved in the pathogenic process of HSP and play a protective role in the development of the disease.
Subject(s)
Humans , Interleukin-27 , Leukocytes, Mononuclear , Patients , IgA Vasculitis , Th17 CellsABSTRACT
Acute kidney injury (AKI), associated with significant morbidity and mortality, is widely known to involve epithelial apoptosis, excessive inflammation, and fibrosis in response to ischemia or reperfusion injury, which results in either chronic pathological changes or death. Therefore, it is imperative that investigations are conducted in order to find effective, early diagnoses, and therapeutic targets needed to help prevent and treat AKI. However, the mechanisms modulating the pathogenesis of AKI still remain largely undetermined. MicroRNAs (miRNAs), small non-coding RNA molecules, play an important role in several fundamental biological and pathological processes by a post transcriptional regulatory function of gene expression. MicroRNA-21 (miR-21) is a recently identified, typical miRNA that is functional as a regulator known to be involved in apoptosis as well as inflammatory and fibrotic signaling pathways in AKI. As a result, miR-21 is now considered a novel biomarker when diagnosing and treating AKI. This article reviews the correlative literature and research progress regarding the roles of miR-21 in AKI.