scholarly journals Protective Effect of Rifampicin Loaded by HPMA-PLA Nanopolymer on Macrophages Infected with Mycobacterium Tuberculosis

2022 ◽  
Vol 2022 ◽  
pp. 1-9
Author(s):  
Guoping Yang ◽  
Guofu Wang ◽  
Liting Liu ◽  
Kaixin Zhai ◽  
Xiaowen Chen ◽  
...  
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Protective Effect ◽  
Cell Model ◽  
Bacterial Activity ◽  
Inflammatory Factors ◽  
Enzyme Linked Immunosorbent Assay ◽  
Protective Mechanism ◽  
Related Factors ◽  
Apoptosis Rate ◽  
In Cells

Purpose. This research was designed to investigate the protective effect of rifampicin (RIF) loaded by N-(2-hydroxypropyl) methylacrylamide- (HPMA-) polylactic acid (PLA) nanopolymer on macrophages infected with Mycobacterium tuberculosis (MTB). Methods. We first induced H37Rv to infect macrophages to build a cell model. Then, the HPMA-PLA nanopolymer loaded with RIF was prepared to treat MTB-infected macrophages. The macrophage activity was tested by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, the nitric oxide (NO) in cells was measured through Griess reagent, and the bacterial activity of MTB was observed via the colony-forming unit (CFU) assay. The inflammation-related factors in cells were detected via the enzyme-linked immunosorbent assay (ELISA), the apoptosis of macrophages was examined via flow cytometry, and the expression of apoptosis-related proteins was determined by western blot (WB). Results. HPMA-PLA had no obvious toxicity to macrophages. The expression of NO and inflammatory factors in macrophages infected with MTB increased significantly, but the apoptosis rate was not significantly different from that of uninfected cells. However, after treatment with HPMA-PLA-RIF or free RIF, the inflammatory reaction of infected cells was inhibited, the expression of NO was decreased, the apoptosis rate was increased, and the bacterial activity in cells was decreased, with statistically significant differences; moreover, HPMA-PLA-RIF was more effective than free RIF. Conclusions. HPMA-PLA-RIF has a high protective effect on macrophages infected with MTB, with high safety. Its protective mechanism is at least partly through inhibiting the production of NO and inflammatory response, which can inhibit bacterial activity and induce cell apoptosis.

scholarly journals miR-124-3p Inhibits Microglial Secondary Inflammation After Basal Ganglia Hemorrhage by Targeting TRAF6 and Repressing the Activation of NLRP3 Inflammasome

2021 ◽  
Vol 12 ◽  
Author(s):  
Yudan Fang ◽  
Xiaoqin Hong
Keyword(s):  
Basal Ganglia ◽  
Cell Viability ◽  
Healthy Volunteers ◽  
Nlrp3 Inflammasome ◽  
Cell Model ◽  
Expression Patterns ◽  
Cell Activity ◽  
Inflammatory Factors ◽  
High Morbidity ◽  
Apoptosis Rate

Objectives: Intracerebral hemorrhage (ICH) represents a serious central nervous system emergency with high morbidity and mortality, and the basal ganglia is the most commonly affected brain region. Differentially expressed microRNAs (miRs) have recently been highlighted to serve as potential diagnostic biomarkers and therapeutic targets for ICH. This study investigated the mechanism of miR-124-3p in microglial secondary inflammation after ICH.Methods: In this study, 48 patients with primary basal ganglia ICH and 48 healthy volunteers were selected and venous blood was collected from all patients on the second morning of admission (within 24 h of stroke onset). The expression of miR-124-3p in serum was detected by RT-qPCR. Three months after ICH, the patients were assessed by modified Rankin Scale (mRS), and the correlation between miR-124-3p expression and mRS score was analyzed by Pearson. The inflammatory response of microglia was induced by lipopolysaccharide (LPS) to establish the cell model of microglial inflammation. miR-124-3p expression patterns were detected in the serum of ICH patients and healthy volunteers, normal microglia, and LPS-induced microglia. The miR-124-3p mimic was transfected into LPS-induced microglia, followed by measurement of the inflammatory factors, apoptosis rate, and cell viability. The target gene of miR-124-3p was predicted and verified. The expression patterns of tumor necrosis factor receptor-associated factor 6 (TRAF6) were detected. pcDNA3.1 and pcDNA3.1-TRAF6 were transfected into LPS-induced HMC3 cells, and nucleotide-binding oligomerization domain-like receptor (NLR) pyrin domain-containing 3 (NLRP3) expression patterns were determined. Lastly, the effects of TRAF6 overexpression on apoptosis, cell viability, and inflammation in HMC3 cells were measured.Results: miR-124-3p was downregulated in the serum of basal ganglia ICH patients and LPS-induced microglia, and miR-124-3p expression was negatively correlated with mRS. Overexpression of miR-124-3p reduced the inflammatory factors and apoptosis rate and promoted cell activity in LPS-induced microglia. miR-124-3p was found to target TRAF6. Overexpression of TRAF6 enhanced the expression of NLRP3 inflammasome, inflammatory factors and apoptosis rate, and reduced cell viability.Conclusion: Our findings indicate that miR-124-3p repressed the activation of NLRP3 inflammasome by targeting TRAF6, thus inhibiting microglial secondary inflammation after ICH in basal ganglia.

Effect of Edaravone on MicroRNA Expression in Exosomes after Hepatic Ischemia-reperfusion Injury

2021 ◽  
Vol 14 ◽  
Author(s):  
Yanxia Fei ◽  
Jiali Shao ◽  
Ge Huang ◽  
Lijuan Wang ◽  
Shuangfa Zou ◽  
...  
Keyword(s):  
Protective Effect ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Quantitative Polymerase Chain Reaction ◽  
Inflammatory Factors ◽  
Enzyme Linked Immunosorbent Assay ◽  
Hepatic Ischemia ◽  
Second Generation Sequencing ◽  
Hepatic Ischemia Reperfusion

Background and Objective: Hepatic ischemia-reperfusion injury (HIRI) results in serious complications after liver resection and transplantation. Edaravone (ED) has a protective effect on IRI. This study was designed to evaluate whether ED could protect the liver of rats from HIRI injury and explored its exosomal miRNA-related mechanism. Methods: The sham group, hepatic ischemia/reperfusion (IR group), and hepatic ischemia/reperfusion + edaravone (ED group) models were established. We determined the protective effect of ED by measuring alanine aminotransferase (ALT), aspartate aminotransferase (AST), malondialdehyde (MDA), superoxide dismutase (SOD); enzyme-linked immunosorbent assay for tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β); hematoxylin-eosin staining and immunohistochemistry for histopathological changes. Exosomal miRNAs were subjected to second-generation sequencing to identify their differential expression. The results were analyzed using bioinformatics methods and validated using real-time quantitative polymerase chain reaction (RT-qPCR). Results: HIRI rats showed higher levels of ALT, AST, oxidative stress, and inflammatory markers; ED attenuated these effects. The sequencing results showed 6 upregulated and 13 downregulated miRNAs in the IR vs. sham groups, 10 upregulated and 10 downregulated miRNAs in the ED vs. IR groups. PC-3p-190-42101 was screened as an overlapping differentially expressed miRNA, and RT-qPCR validation showed that its expression in HIRI rats was significantly decreased; ED prevented this downregulation. Moreover, the expression of PC-3P-190-42101 was significantly correlated with the level of inflammatory factors. Conclusion: These findings indicate that ED can regulate the level of inflammatory factors by affecting the expression of miRNA PC-3p-190-42101 in plasma exosomes to protect the liver from IRI.

scholarly journals Electroacupuncture Alleviates Inflammation of Dry Eye Diseases by Regulating the α7nAChR/NF-κB Signaling Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-15
Author(s):  
Ning Ding ◽  
Qingbo Wei ◽  
Weimin Deng ◽  
Xinyi Sun ◽  
Jie Zhang ◽  
...  
Keyword(s):  
Protective Effect ◽  
Signaling Pathway ◽  
Dry Eye ◽  
Inhibitory Effect ◽  
Cell Ultrastructure ◽  
Inflammatory Factors ◽  
Enzyme Linked Immunosorbent Assay ◽  
Scopolamine Hydrobromide ◽  
Beneficial Effects ◽  
Chip Technology

Purpose. We tried to investigate whether electroacupuncture (EA) can reduce inflammation of dry eye disease (DED) by regulating α7nAChR and inhibiting the NF-κB signaling pathway. Methods. Healthy New Zealand white rabbits were treated with scopolamine hydrobromide (Scop) for 21 consecutive days to establish the DED animal model. After 21 days, EA, fluorometholone (Flu), and α7nAChR antagonist (α-BGT) treatments were performed, and the Scop injection was continued until day 35. During treatment, the fluorescence staining of the corneal epithelium and the level of tear flow were observed. The influence of EA on the LG pathology and inflammatory factors ACh, α7nAChR, and NF-κB was detected using the LG histopathology, transmission electron microscopy (TEM), cytokine protein chip technology, enzyme-linked immunosorbent assay (ELISA), and Western blot. Results. The EA stimulation can reduce the corneal epithelial damage and repair epithelial cell ultrastructure, promote the tear secretion, relieve the LG atrophy and decrease lipid droplet accumulation in LG acinar cell, and reduce the levels of inflammatory cytokines (i.e., IL-1, MIP-1b, TNF-α, and IL-8) in the LG. The protective effect of EA on the inflammation and the ocular surface is similar to the corticosteroid Flu. EA and Flu can upregulate the expression of the α7nAChR and downregulate the expression of NF-κB. The α7nAChR antagonist α-BGT can reverse the protective effect of EA on the LG and the inhibitory effect on the NF-κB pathway and the expression of inflammatory factors but cannot affect the expression of Flu on the NF-κB pathway and inflammatory factors. Conclusion. These results prove that EA can alleviate DEDs by stimulating the acupoints around the eyes. These beneficial effects are related to the upregulation of α7nAChR and the downregulation of NF-κB in the LG. The protective effect of LG is mediated through the anti-inflammatory pathway mediated by α7nAChR. EA can reduce the NF-κB P65 nuclear transcription and reduce inflammatory factors by regulating α7nAChR. This expression indicates that the α7nAChR/NF-κB signaling pathway may serve as a potential therapeutic target for EA to treat DEDs.

scholarly journals Co-treatment with disulfiram and glycyrrhizic acid suppresses the inflammatory response of chondrocytes

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Chao Li ◽  
Li Li ◽  
Tian Lan
Keyword(s):  
Cell Proliferation ◽  
Inflammatory Response ◽  
Glycyrrhizic Acid ◽  
Cell Model ◽  
High Mobility ◽  
Cell Counting ◽  
Inflammatory Factors ◽  
Enzyme Linked Immunosorbent Assay ◽  
High Concentration ◽  
Protein Levels

Abstract Background Osteoarthritis (OA) is a kind of systemic musculoskeletal disorder and a most important factor for causing disability and physical painfulness. Nevertheless, due to the fact that OA can be triggered by multiple etiological factors, this disease is hard to be cured. Therefore, it is of great necessity for us to find novel targets or drugs for OA treatment. Materials and methods The chondrocytes were treated with lipopolysaccharide (LPS) and adenosine triphosphate (ATP) to induce pyroptosis in OA. The cell proliferation was detected by Cell Counting Kit-8 assay (CCK-8 assay). Enzyme-linked immunosorbent assay (ELISA) was used for the detection of pyroptosis-related inflammatory factors. Then, the antagonists for gasdermin D (GSDMD) (disulfiram) and high mobility group box 1 (HMGB1) (glycyrrhizic acid) were used to treat the cell model to observe the effects of disulfiram and glycyrrhizic acid on the proliferation of chondrocytes in OA. The protein levels of pyroptosis-related inflammatory factors were measured by western blot, and the levels of aldehyde dehydrogenase (ALDH) and reactive oxygen species (ROS) were measured by corresponding commercial kits. Results After chondrocytes were induced by LPS and ATP, the cell proliferation was decreased and the expressions of pyroptosis-related inflammatory factors were increased. Disulfiram and glycyrrhizic acid treatment led to enhanced cell proliferation and increased expressions of pyroptosis-related inflammatory factors, while disulfiram showed better alleviative effects on the inflammation in chondrocytes in OA. However, co-treatment with disulfiram at a high concentration and glycyrrhizic acid did not result in higher proliferation of chondrocytes and alleviated inflammation, but led to oxidative stress. Conclusion In conclusion, co-treatment with disulfiram and glycyrrhizic acid at a standard concentration suppresses the inflammatory response of chondrocytes, which may provide guidance for the use of the drugs in the treatment of OA.

Down-regulation of MiR-138-5p Protects Chondrocytes ATDC5 and CHON-001 from IL-1 β-induced Inflammation Via Up-regulating SOX9

2020 ◽  
Vol 25 (43) ◽  
pp. 4613-4621 ◽  
Author(s):  
He Chunlei ◽  
Zhao Chang ◽  
Liu Sheng ◽  
Zhong Yanchun ◽  
Liu Lulin ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
High Mobility ◽  
Luciferase Assay ◽  
Inflammatory Factors ◽  
Chondrocyte Apoptosis ◽  
Enzyme Linked Immunosorbent Assay ◽  
Promoting Effect ◽  
Related Factors ◽  
And Migration ◽  
Proliferation And Migration

Background: Osteoarthritis (OA) pertains to a chronic disease of degenerative joints distinguished by articular cartilage destruction, subchondral bone remodeling, osteophyte formation, and inflammatory changes. Chondrocyte apoptosis is inextricably linked to cartilage degeneration. SRY-related high-mobility-group-box 9 (SOX9) is a well-acknowledged transcription factor in the chondrogenesis. Nevertheless, the detailed function of miR-138-5p/SOX9 in OA remains to be fully clarified. Materials and Methods: qRT-PCR was performed to measure the expressions of miR-138-5p and SOX9 mRNA in OA and normal cartilage tissues and cells. Human chondrocyte cell lines, CHON-001 and ATDC5, were treated with different doses of interleukin-1β (IL-1β) to simulate the inflammatory response environment of OA. miR-138-5p mimics, miR-138-5p inhibitors, and SOX9 small interfering RNA (siRNA) were constructed and transfected into CHON-001 and ATDC5 cells. CCK-8 was conducted to determine the cell viability and transwell assay was used to monitor the migration of cells. Western blot was carried out to detect the expressions of apoptosis- related factors. Enzyme-linked immunosorbent assay (ELISA) was adopted to measure the contents of inflammatory factors. TargetScan predicted SOX9 was a target gene of miR-138-5p, which was then verified by luciferase assay. Results: miR-138-5p expression was down-regulated in OA and regulated SOX9 expression. The downregulation of miR-138-5p facilitated the proliferation and migration of CHON-001 and ATDC5 cells, while impeded their apoptosis and inflammatory response. Besides, down-regulated SOX9 can counteract the promoting effect of down-regulated miR-138-5p on the proliferation and migration of chondrocytes. Conclusion: miR-138-5p can arrest the proliferation and migration of CHON-001 and ATDC5 via restraining SOX9, and facilitate the apoptosis and inflammation. This study revealed the protective effect of down-regulated miR-138-5p on the inflammatory injury of chondrocytes caused by IL-1β.

scholarly journals MiR-20a-5p Regulates MPP+-Induced Oxidative Stress and Neuroinflammation in HT22 Cells by Targeting IRF9/NF-κB Axis

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Qiang Wang ◽  
Yuan Wang ◽  
Feng Zhou ◽  
Jie Li ◽  
Gang Lu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Damage ◽  
Annexin V ◽  
Cell Counting ◽  
Inflammatory Factors ◽  
Enzyme Linked Immunosorbent Assay ◽  
Related Factors ◽  
Ht22 Cells ◽  
Mitochondrial Disruption ◽  
And Oxidative Stress

Substantial evidence indicates that microRNAs (miRNAs) can be used as biological markers of Parkinson’s disease (PD) and contribute to the risk assessment, early diagnosis, and treatment. We aimed to explore the role and potential mechanism of miR-20a-5p on inflammation and oxidative stress in 1-methyl-4-phenyl pyridine ion- (MPP+-) induced HT22 cells. HT22 cells were pretreated with miR-20a-5p mimic and/or pcDNA-IRF9 for 24 h and then treated with MPP+ (0.5 mM) for 24 h. The cell viability and apoptosis were determined using the Cell Counting Kit-8 (CCK-8) and Annexin V FITC/PI staining flow cytometry assay, respectively. The expression and secretion of inflammatory factors and oxidative stress-related factors were detected by enzyme-linked immunosorbent assay (ELISA). The protein expression levels were detected using Western blot analysis. Here, we discovered that MPP+ led to mitochondrial dysfunction, inflammation, and cell damage of HT22 cells, which were alleviated by miR-20a-5p overexpression. We further clarified that interferon regulatory factor 9 (IRF9) was a target gene of miR-20a-5p. IRF9 contributed to MPP+-induced mitochondrial disruption, inflammation, and cell apoptosis. Moreover, IRF9 hindered the improvement of miR-20a-5p overexpression on MPP+-induced neurotoxicity. Furthermore, the decrease of p-P65 level induced by miR-20a-5p mimic was significantly reversed by IRF9 overexpression. These findings demonstrate that miR-20a-5p contributes to MPP+-induced mitochondrial disruption and cell damage, and miR-20a-5p might be a novel therapeutic target for PD.

scholarly journals Bacoside-A exerts protective effect against Parkinson’s disease-induced functional damage in mice via inhibition of apoptosis and oxidative response

2021 ◽  
Vol 19 (12) ◽  
pp. 2565-2570
Author(s):  
Binbin Zhang ◽  
Jiankuan Shi ◽  
Lei Chang ◽  
Hong Wang ◽  
Yaping Wang ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cytochrome C ◽  
Parkinson Disease ◽  
Protective Effect ◽  
Rat Model ◽  
Neuronal Degeneration ◽  
Inflammatory Factors ◽  
Enzyme Linked Immunosorbent Assay ◽  
Bacoside A

Purpose: To determine the effect of bacoside-A on Parkinson's disease (PD) in a rat model, and elucidate its mechanism of action.Methods: A rat model of PD was established by administration of 5 µL of 6-hydroxydopamine in ascorbic acid (0.1 %). Measurement of serum levels of inflammatory factors was carried out using enzyme-linked immunosorbent assay (ELISA) kits. Western blotting was used to assay Bax, cytochrome c and Bcl-2 in rat hippocampus.Results: Bacoside-A treatment significantly reduced PD-induced high turning values in rats (p < 0.05). Treatment with bacoside-A reversed PD-mediated suppression of serum activities of CAT and glutathione peroxidase (GPx). In bacoside-A-treated PD rats, dose-dependent suppression of acetylcholinesterase (AChE) and inducible nitric oxide synthase (iNOS) activities were observed (p < 0.05). Bacoside-A-treated PD rats significantly (p < 0.018) reduced interleukin (IL)-1β and IL-6 levels. Treatment of PD rats with bacoside-A effectively reduced levels of tumor necrosis factor (TNF)-α, NF-κB p65, (COX)-2 and p53 protein, and also reversed up-regulations of Bax, cytochrome C, caspase-3 and caspase-9.Conclusion: Bacoside-A exhibits a protective effect against Parkinson disease-induced oxidative damage and neuronal degeneration in rats through downregulation of iNOS, AChE, inflammatory cytokines and pro-apoptotic proteins. Therefore, bacoside-A has potentials for use in the management of Parkinson disease. Keywords: Parkinson disease, Neuroprotective, Pro-apoptotic, Cytokines, Neurotoxicity

scholarly journals The Protective Effect of E. faecium on S. typhimurium Infection Induced Damage to Intestinal Mucosa

2021 ◽  
Vol 8 ◽  
Author(s):  
Hang Zhang ◽  
Minjuan Wang ◽  
Junpeng Jia ◽  
Jiayi Zhao ◽  
Stoffel Matjeke Radebe ◽  
...  
Keyword(s):  
Protective Effect ◽  
Salmonella Typhimurium ◽  
Intestinal Mucosa ◽  
Enterococcus Faecium ◽  
Intestinal Morphology ◽  
Inflammatory Factors ◽  
Economic Losses ◽  
Protective Mechanism ◽  
Inflammatory Factor ◽  
Alternative Treatment Option

Intensive farming is prone to induce large-scale outbreaks of infectious diseases, with increasing use of antibiotics, which deviate from the demand of organic farming. The high mortality rate of chickens infected with Salmonella caused huge economic losses; therefore, the promising safe prevention and treatment measures of Salmonella are in urgent need, such as probiotics. Probiotics are becoming an ideal alternative treatment option besides antibiotics, but the effective chicken probiotic strains with clear protective mechanism against Salmonella remain unclear. In this study, we found Enterococcus faecium YQH2 was effective in preventing Salmonella typhimurium infection in chickens. Salmonella typhimurium induced the loss of body weight, and liver and intestinal morphology damage. The inflammatory factor levels increased and intestinal proliferation inhibited. However, after treatment with Enterococcus faecium YQH2, broilers grew normally, the pathological changes of liver and intestine were reduced, and the colonization of Salmonella in the intestine was improved. Not only that, the length of villi and the depth of crypts were relatively normal, and the levels of inflammatory factors such as IL-1β, TNF-α, and IL-8 were reduced. The number of PCNA cells of Enterococcus faecium YQH2 returned to normal under the action of Salmonella typhimurium infection, which was conducive to the normal proliferation of intestinal epithelial cells. The protective effect of Enterococcus faecium YQH2 may be due to the attribution to the activation of hypoxia and then induced the proliferation of intestinal stem cells to repair the damage of intestinal mucosa under Salmonella typhimurium infection. This study demonstrated that Enterococcus faecium YQH2 was effective in preventing Salmonella typhimurium infection, which could be further used in the chicken health breeding.

scholarly journals Effect of bone morphogenetic protein-2 on diabetic retinopathy and its mechanism of action

2021 ◽  
Vol 18 (5) ◽  
pp. 1069-1076
Author(s):  
Zaohe Sun ◽  
Guangming Wan ◽  
Shenzhi Liang ◽  
Cheng Qian
Keyword(s):  
Bone Morphogenetic Protein ◽  
Retinal Pigment ◽  
Retinal Pigment Epithelial Cells ◽  
Bone Morphogenetic Protein 2 ◽  
Cell Counting ◽  
Inflammatory Factors ◽  
Enzyme Linked Immunosorbent Assay ◽  
Vascular Endothelial ◽  
Related Factors ◽  
Morphogenetic Protein

Purpose: To investigate the effect of bone morphogenetic protein-2 (BMP-2) on human retinal vascular endothelial cells (RECs) and human retinal pigment epithelial cells (RPE) cultured in high glucose (HG) in vitro, and the underlying mechanism. Methods: Cell counting kit-8 (CCK-8) was used to determine cell proliferation while Western blot was used to assay the expressions of extracellular matrix and angiogenesis-related factors, Expressions of cytokines and chemokines were assessed by quantitative real time polymerase chain reaction (qRTPCR) and enzyme-linked immunosorbent assay (ELISA). Changes in Smad, ERK, JNK and p38MAPK signal pathway were measured by transfection and interference. Results: The level of expression of BMP-2 in HG group was higher than that in normal glucose (NG) culture group. The expressions of angiogenesis-related factors i.e. vascular endothelial growth factor (VEGF) and intercellular cell adhesion molecule-1 (ICAM1), pro-inflammatory factors i.e. IL-6 and chemokine monocyte chemokine protein-1 (MCP1), increased significantly in HG group compared to NG and HG + BMP-2 groups. Phosphorylation of Smad1/5/8 and activation of ERK, JNK and p38MAPK signaling pathways were enhanced by BMP-2. Conclusion: These results suggest that BMP-2 promotes angiogenesis and enhances the expressions of inflammatory cytokines via Smad signaling pathway.

Expression and Significance of Th17 Cells and Related Factors in Patients with Autoimmune Hepatitis

2019 ◽  
Vol 22 (4) ◽  
pp. 232-237 ◽  
Author(s):  
Jihong An
Keyword(s):  
Autoimmune Hepatitis ◽  
Peripheral Blood ◽  
Th17 Cells ◽  
Treg Cells ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Serum Total Bilirubin ◽  
Study Group ◽  
Related Factors ◽  
Tnf Α

Objective: This study aims to investigate the expression and clinical significance of Th17 cells and related factors in peripheral blood of patients with Autoimmune Hepatitis (AIH). Methods: A retrospective selection of 100 patients with AIH were included as a study group, and 100 healthy volunteers in the outpatient clinic were selected as the control group. The levels of IL- 17, IL-6, IL-21 and TNF-α in peripheral blood of all subjects were detected by enzyme-linked immunosorbent assay and the frequency of Th17 cells and Treg cells was detected by flow cytometry. Results: Results showed that the study group had higher levels of serum total bilirubin (TBil), alkaline phosphatase (ALP), γ -glutamyltranspeptidase (γ-GT), immunoglobulin G (IgG), immunoglobulin M (IgM), alanine aminotransferase (ALT) and aspartate aminotransferase (AST) than the control group, as well as higher levels of IL-17, IL-6, IL-21 and TNF-α in serum. The frequency of Th17 cells in peripheral blood was higher in the study group, while the frequency of Treg cells was lower. Also, serum IL-17, TNF-α levels and Th17 cells frequency were positively correlated with ALT and AST, whereas Treg cells frequency were negatively correlated with ALT and AST levels. Conclusion: Our finding demonstrates that Th17 cell frequency and their related factors IL-17 and TNF-α, are associated with liver damage, which might be used to monitor AIH disease severity.

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