ArticleBioengineered2021
Zhike Pingchuan Granule suppresses interleukin (IL)-6 or the medium of M2 macrophages induced apoptosis in human bronchial epithelial cells.
Article in Bioengineered, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed, 3 citations in OpenAlex.
- A multi-omics Mendelian randomization identifies putatively causal genes and DNA methylation sites for asthma.The World Allergy Organization journal · 2024Article
- Article
- Supplementation with paraformic acid in the diet improved intestinal development through modulating intestinal inflammation and microbiota in broiler chickens.Frontiers in microbiology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of this study was to explore the effects and action mechanism of Zhike Pingchuan Granule in human bronchial epithelial cells induced by IL-6 or the supernatant of M2. Upon IL-6 stimulation at different doses, Cell Counting Kit-8 (CCK8) assay and flow cytometry were, respectively, utilized to detect the cell viability and apoptosis levels of 16-HBE cells. ELISA and Western blot were, respectively, used to analyze the inflammatory markers and JAK2/STAT3 signals. Immunofluorescence assay was performed to identify M0 and M2 cells. As shown in results, ZKPC perturbed the expression of IL-6 inducible genes important for apoptosis, oxidative and inflammatory response, which was enhanced by JAK2 inhibitor. Besides the inhibitory effects on the phosphorylation levels of JAK2/STAT3, ZKPC markedly increased cell viability and reduced apoptosis in human bronchial epithelial cells (16-HBE) cultured in the supernatant of M2 cells. Collectively, ZKPC could inhibit the IL-6-induced JAK/STAT3 signaling cascade, increase cell viability and decrease apoptosis induced by the supernatant of M2. A more comprehensive understanding of the action mechanism of ZKPC on JAK2/STAT3 signaling pathway in human bronchial epithelial cells induced by IL-6 or M2 supernatant will enable ZKPC development in the control of asthma.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.