scholarly journals Aerobic Exercise Inhibits Inflammatory Response in Atherosclerosis via Sestrin1 Protein

2021 ◽  
Author(s):  
yunfeng sun ◽  
ke Li ◽  
wei wu ◽  
keping yang
Keyword(s):  
Inflammatory Response ◽  
Aerobic Exercise ◽  
Aerobic Training ◽  
Development Stage ◽  
Pathological Process ◽  
Expression Level ◽  
Inflammatory Factors ◽  
Tnf Α ◽  
Anti Inflammation ◽  
High Expression Level

Abstract Background Aerobic exercise plays an important role in prevention and treatment of atherosclerosis but its role in inflammatory response is not completely clear. Inflammatory response is the main pathological process during occurrence and development stage of atherosclerosis. SESNs are considered as anti-inflammation protein in atherosclerosis. Results In current study, a high expression level of SESN1 is identified under the condition of aerobic exercise, further investigation shows levels of IL-1β/IL-6/TNF-α are significantly suppressed compared to those atherosclerosis mice with no aerobic training. Besides, we find that the activation of NK-κB signaling is impeded. Combine with our previous study, SESN1 is considered as the downstream factor of aerobic exercise which tend to inhibit the activation of inflammatory signaling and result in suppress the expression level of inflammatory factors. Another exciting finding is that MMP9/13 are also suppressed，but the potential mechanism is unclear. Conclusion Overall, present study sheds light on the significance of aerobic exercise for inflammation and stability of plaque through SESN1 may help developing new clinical treatments of atherosclerosis.

scholarly journals Aerobic Exercise Inhibits CUMS-Depressed Mice Hippocampal Inflammatory Response via Activating Hippocampal miR-223/TLR4/MyD88-NF-κB Pathway

2020 ◽  
Vol 17 (8) ◽  
pp. 2676 ◽  
Author(s):  
Honglin Qu ◽  
Ruilian Liu ◽  
Jiaqin Chen ◽  
Lan Zheng ◽  
Rui Chen
Keyword(s):  
Inflammatory Response ◽  
Aerobic Exercise ◽  
Exercise Group ◽  
Inflammatory Factors ◽  
Control Group ◽  
Mild Stress ◽  
Hippocampal Function ◽  
Model Group ◽  
Mice Model ◽  
Protein Levels

Objective: To investigate the role of aerobic exercise in inhibiting chronic unpredictable mild stress (CUMS) depressed mice hippocampal inflammatory response and its potential mechanisms. Methods: Fifty-four male eight-week-old C57BL/6 mice were divided as control group (CG) (18 mice) and model group (36 mice). Model group mice were treated with 13 chronic stimulating factors for 28 days to set up the CUMS depression model. Neurobehavioral assessment was performed after modeling. The mice in the model group were randomly divided into the control model group (MG) and the aerobic exercise group (EG), with 18mice in each group. The EG group carried out the adaptive training of the running platform: 10 m/min, 0° slope, and increased by 10 minutes per day for 6 days. The formal training was carried for 8 weeks with 10 m/min speed, 0° slope, 60 min/d, 6 d/Week. After the training, a neurobehavioral assessment was performed, and hippocampus IL-1β and IL-10 protein levels were detected by ELISA. RT–PCR was used to detect the expression of miR-223 and TLR4, MyD88, and NF-κB in the hippocampus. Western blot was used to detect the expression of TLR4 and phosphorylated NF-κBp65 protein in the hippocampus. Results: The hippocampus function of CUMS depression model mice was impaired. The forced swimming and forced tail suspension time were significantly prolonged, and inflammatory factors IL-1β were significantly increased in the hippocampus. Aerobic exercise significantly improves CUMS-depressed mice hippocampal function, effectively reducing depressive behavior and IL-1β levels, and increasing IL-10 levels. Besides, aerobic exercise significantly upregulates the expression level of miR-223 and inhibits the high expression of TLR4, MyD88, and NF-κB. Conclusion: Aerobic exercise significantly increases the CUMS-depressed mice hippocampus expression of miR-223, and inhibits the downstream TLR4/MyD88-NF-κB signaling pathway and the hippocampal inflammatory response, which contributes to the improvement of the hippocampal function.

scholarly journals Daphnetin inhibits proliferation and inflammatory response in human HaCaT keratinocytes and ameliorates imiquimod-induced psoriasis-like skin lesion in mice

2020 ◽  
Vol 53 (1) ◽  
Author(s):  
Jintao Gao ◽  
Fangru Chen ◽  
Huanan Fang ◽  
Jing Mi ◽  
Qi Qi ◽  
...  
Keyword(s):  
Skin Lesion ◽  
Inflammatory Response ◽  
Mouse Model ◽  
Nuclear Translocation ◽  
Marker Gene ◽  
Inflammatory Factors ◽  
Mrna Levels ◽  
Hacat Keratinocytes ◽  
Tnf Α

Abstract Background Psoriasis is a common chronic inflammatory skin disease. Keratinocytes hyperproliferation and excessive inflammatory response contribute to psoriasis pathogenesis. The agents able to attenuate keratinocytes hyperproliferation and excessive inflammatory response are considered to be potentially useful for psoriasis treatment. Daphnetin exhibits broad bioactivities including anti-proliferation and anti-inflammatory. This study aims to evaluate the anti-psoriatic potential of daphnetin in vitro and in vivo, and explore underlying mechanisms. Methods HaCaT keratinocytes was stimulated with the mixture of IL-17A, IL-22, oncostatin M, IL-1α, and TNF-α (M5) to establish psoriatic keratinocyte model in vitro. Cell viability was measured using Cell Counting Kit-8 (CCK-8). Quantitative Real-Time PCR (qRT-PCR) was performed to measure the mRNA levels of hyperproliferative marker gene keratin 6 (KRT6), differentiation marker gene keratin 1 (KRT1) and inflammatory factors IL-1β, IL-6, IL-8, TNF-α, IL-23A and MCP-1. Western blotting was used to detect the protein levels of p65 and p-p65. Indirect immunofluorescence assay (IFA) was carried out to detect p65 nuclear translocation. Imiquimod (IMQ) was used to construct psoriasis-like mouse model. Psoriasis severity (erythema, scaling) was scored based on Psoriasis Area Severity Index (PASI). Hematoxylin and eosin (H&E) staining was performed to examine histological change in skin lesion. The expression of inflammatory factors including IL-6, TNF-α, IL-23A and IL-17A in skin lesion was measured by qRT-PCR. Results Daphnetin attenuated M5-induced hyperproliferation in HaCaT keratinocytes. M5 stimulation significantly upregulated mRNA levels of IL-1β, IL-6, IL-8, TNF-α, IL-23A and MCP-1. However, daphnetin treatment partially attenuated the upregulation of those inflammatory cytokines. Daphnetin was found to be able to inhibit p65 phosphorylation and nuclear translocation in HaCaT keratinocytes. In addition, daphnetin significantly ameliorate the severity of skin lesion (erythema, scaling and epidermal thickness, inflammatory cell infiltration) in IMQ-induced psoriasis-like mouse model. Daphnetin treatment attenuated IMQ-induced upregulation of inflammatory cytokines including IL-6, IL-23A and IL-17A in skin lesion of mice. Conclusions Daphnetin was able to attenuate proliferation and inflammatory response induced by M5 in HaCaT keratinocytes through suppression of NF-κB signaling pathway. Daphnetin could ameliorate the severity of skin lesion and improve inflammation status in IMQ-induced psoriasis-like mouse model. Daphnetin could be an attractive candidate for future development as an anti-psoriatic agent.

Comparing the effect of intestinal bacteria from rabbit, pig, and chicken on inflammatory response in cultured rabbit crypt and villus

2019 ◽  
Vol 65 (1) ◽  
pp. 59-67 ◽  
Author(s):  
Hong Xiao Cui ◽  
Xiu Rong Xu
Keyword(s):  
Inflammatory Response ◽  
Inflammatory Responses ◽  
Intestinal Bacteria ◽  
Inflammatory Factors ◽  
Rabbit Ileum ◽  
Necrosis Factor Alpha ◽  
Heat Treated ◽  
Tnf Α ◽  
Factor Alpha ◽  
Anti Inflammatory

Rabbit is susceptible to intestinal infection, which often results in severe inflammatory response. To investigate whether the special community structure of rabbit intestinal bacteria contributes to this susceptibility, we compared the inflammatory responses of isolated rabbit crypt and villus to heat-treated total bacteria in pig, chicken, and rabbit ileal contents. The dominant phylum in pig and chicken ileum was Firmicutes, while Bacteroidetes was dominant in rabbit ileum. The intestinal bacteria from rabbit induced higher expression of toll-like receptor 4 (TLR4) in rabbit crypt and villus (P < 0.05). TLR2 and TLR3 expression was obviously stimulated by chicken and pig intestinal bacteria (P < 0.05) but not by those of rabbit. The ileal bacteria from those three animals all increased the expression of tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6) in crypts and villus (P < 0.05). Chicken and pig ileal bacteria also stimulated the expression of anti-inflammatory factors interferon beta (IFN-β) and IL-10 (P < 0.05), while those of rabbit did not (P > 0.05). In conclusion, a higher abundance of Gram-negative bacteria in rabbit ileum did not lead to more expressive pro-inflammatory cytokines in isolated rabbit crypt and villus, but a higher percentage of Lactobacillus in chicken ileum might result in more expressive anti-inflammatory factors.

scholarly journals Echinacoside Improves Cognitive Impairment by Inhibiting Aβ Deposition Through the PI3K/AKT/Nrf2/PPARγ Signaling Pathways in APP/PS1 Mice

2021 ◽  
Author(s):  
hui qiu ◽  
min xue liu
Keyword(s):  
Signaling Pathway ◽  
Escape Latency ◽  
Senile Plaques ◽  
Pathological Process ◽  
Tnf Α ◽  
Nrf2 Signaling Pathway ◽  
Ros Formation ◽  
The Times ◽  
The Brain ◽  
Anti Inflammation

Abstract Echinacoside (ECH), a phenylethanoid glycoside, has protective activity in neurodegenerative disease, including anti-inflammation and antioxidation. However, the effects of ECH in Alzheimer’s disease (AD) are not very clear. This present study investigates the role and mechanism of ECH in the pathological process of AD. APP/PS1 mice were treated with ECH in 50 mg/kg/d for 3 months. Morris water maze, nesting test and immunofluorescence staining were used to observe whether ECH could improve AD pathology. Western blot was used to study the mechanism of ECH improving AD pathology. The results showed that ECH alleviated the memory impairment of APP/PS1 mice by reducing the time of escape latency as well as increasing the times of crossing the platform and rescued the impaired ability to construct nests. In addition, ECH significantly reduced the deposition of senile plaques in the brain and decreased the expression of BACE1 in APP/PS1 mice through activating PI3K/AKT/ Nrf2/PPARγ pathway. Furthermore, ECH decreased ROS formation, GP91 and 8-OHdG expression, upregulated the expression of SOD1 and SOD2 as well as activating the PI3K/AKT/Nrf2 signaling pathway. Moreover, ECH inhibited glia cells activation, pro-inflammatory cytokine IL-1β and TNF-α release, NLRP3 inflammasome formation through TXNIP/Trx-1 signaling pathway. In conclusion, this paper reported that ECH improved cognitive function, inhibited oxidative stress and inflammatory response in AD. Therefore, we suggest that ECH may be considered as a potential drug for AD treatment.

Pcsk9 Knockout Aggravated Experimental Apical Periodontitis via LDLR

2021 ◽  
pp. 002203452110151
Author(s):  
L. Huang ◽  
H. Wu ◽  
Y. Wu ◽  
F. Song ◽  
L. Zhang ◽  
...  
Keyword(s):  
Osteoclast Differentiation ◽  
Apical Periodontitis ◽  
Cholesterol Homeostasis ◽  
Expression Level ◽  
Inflammatory Factors ◽  
Tartrate Resistant Acid Phosphatase ◽  
Dependent Manner ◽  
Lps Challenge ◽  
Tnf Α ◽  
Computed Tomography Scanning

Apical periodontitis (AP), an inflammatory lesion around the apex of tooth roots, is mostly caused by dental pulp infection. Proprotein convertase subtilisin/kexin type 9 (PCSK9) plays a vital role in regulating cholesterol homeostasis by targeting low-density lipoprotein receptor (LDLR) and participates in bacterium-induced chronic periodontitis. However, the roles of PCSK9 in AP are unknown. Here, we investigated its role in AP by using Pcsk9−/− mice. Micro–computed tomography scanning and histological staining revealed that the periapical bone loss of Pcsk9−/− mice was greater than that of wild-type (WT) mice, and increased expression of inflammation-related factors tumor necrosis factor α (TNF-α) and interleukin (IL)–6 was also observed. Immunofluorescence staining and quantitative real-time polymerase chain reaction showed PCSK9 expression in bone marrow macrophages (BMMs) was increased after treatment with lipopolysaccharide (LPS). This finding was consistent with the in vivo results that the expression level of PCSK9 in exposed WT mice increased compared with that in unexposed WT mice. After LPS challenge, the expression levels of TNF-α, IL-1β, and IL-6 in BMMs were increased, and Pcsk9 knockout aggravated the expression of these inflammatory factors. The number of osteoclasts positive for tartrate-resistant acid phosphatase staining around the apical lesion in Pcsk9−/− mice was higher than that in WT mice. Then BMMs underwent the osteoclast differentiation. Pcsk9 knockout BMMs induced increased and larger osteoclasts. While this effect of Pcsk9 knockout was abolished by the addition of Ldlr small interfering RNA, revealing that Pcsk9 knockout increased osteoclastogenesis was dependent on the LDLR. Immunohistochemistry staining showed increased expression level of LDLR in exposed Pcsk9−/− periapical areas. In vitro experiments showed that LPS promoted the expression level of LDLR in Pcsk9−/− BMMs and increased osteoclast formation ability, indicating that LPS promoted the elevation of osteoclasteogenesis caused by the Pcsk9 knockout. In conclusion, Pcsk9 deficiency aggravated the inflammatory response and promoted the osteoclastogenesis in an LDLR-dependent manner in AP experimental mice.

scholarly journals Galuteolin suppresses proliferation and inflammation in TNF-α-induced RA-FLS cells by activating HMOX1 to regulate IKKβ/NF-κB pathway

2020 ◽  
Vol 15 (1) ◽  
Author(s):  
Yin Guan ◽  
Xiaoqian Zhao ◽  
Weiwei Liu ◽  
Yue Wang
Keyword(s):  
Cell Proliferation ◽  
Caspase 3 ◽  
Inflammatory Factors ◽  
Tunel Staining ◽  
Dependent Manner ◽  
Protective Effects ◽  
Tnf Α ◽  
Apoptosis And Inflammation ◽  
Dose Dependent ◽  
Anti Inflammation

Abstract Objective Galuteolin (Galu) is a substance extracted and purified from honeysuckle. The purpose of this study was to explore the effects of Galu on the TNF-α-induced RA-FLS cells (synoviocytes) and reveal its potential molecular mechanism from the perspectives of anti-apoptosis and anti-inflammation. Methods After TNF-α stimulation, cell proliferation of RA-FLS was assessed by CCK-8 assay. TUNEL staining was used to detect the apoptosis. Western blot was used to detect the expressions of Iκκβ, p-p65, p65, p-IκB, IκB, Cleaved-caspase3, Caspase-3, Bcl-2, and Bax. HO-1 were determined by RT-PCR. The contents of pro-inflammatory cytokines IL-1β, IL-6, IL-8, and MMP-1 were determined by ELISA. Results Galu significantly suppressed cell proliferation in a dose-dependent manner. Additionally, Galu obviously promotes cell apoptosis rate of RA-FLS cells and elevated the expression levels of HO-1, caspase-3, and Bax, while reducing the expression level of Bcl-2. Furthermore, Galu apparently inhibited the levels of Iκκβ, p-p65, and p-IκB. Moreover, Galu also significantly reduced the levels of pro-inflammatory factors IL-1β, IL-6, IL-8, and MMP-1 in RA-FLS cells. Conclusion Galuteolin exerts protective effects against TNF-α-induced RA-FLS cells by inhibiting apoptosis and inflammation, which can guide the clinical use of rheumatoid arthritis.

scholarly journals Dexmedetomidine reduces inflammation in mice with acute pancreatitis by inhibiting NLRP3 inflammasome and sympathetic nerve activity

2020 ◽  
Vol 19 (5) ◽  
pp. 943-947
Author(s):  
Yanjun Gao ◽  
JinHui Xie ◽  
Ruobin Liu ◽  
Yue Li ◽  
Wenjun Yan
Keyword(s):  
Acute Pancreatitis ◽  
Inflammatory Response ◽  
Nlrp3 Inflammasome ◽  
Sympathetic Nerve ◽  
Pancreatic Tissue ◽  
Inflammatory Factors ◽  
Blood Levels ◽  
Related Factors ◽  
Tnf Α ◽  
Net Protein

Purpose: To study the anti-inflammatory influence of dexmedetomidine (DEX) in mice with acute pancreatitis (AP), and to determine the underlying mechanism.Methods: A total of 75 healthy ICR male mice were randomly divided into control, mild acute pancreatitis (MAP), MAP+DEX, severe acute pancreatitis (SAP), and SAP+DEX groups, with 15 mice/group. Blood levels of inflammatory factors (TNF-α and IL-1β) and norepinephrine were assayed ineach group. Western blotting was used to assay the protein expressions of NLRP3 and norepinephrine transporter (NET) in the pancreatic tissue of each group.Results: The levels of inflammatory factors in the MAP+DEX group were markedly lower than those in the MAP group after 10 h of MAP induction (p < 0.01). Mice in MAP+DEX group had significantly lower expression of NLRP3 in pancreatic tissue, and significantly higher NET protein level, relative to the MAP mice. Following 10 h of SAP, concentrations of the inflammatory factors and the pancreatic expression of NLRP3 were lower in SAP+DEX-treated mice than in SAP mice, while NET protein was significantly higher in SAP mice (p < 0.01).Conclusion: DEX reduces the expressions of inflammation-related factors TNF-α and IL-1β, and inhibits inflammatory response in mice with AP via downregulation of NET protein expression via inhibition of NLRP3 and early sympathetic events. Keywords: Dexmedetomidine, NLRP3 inflammasome, Sympathetic nerve, Acute pancreatitis, Inflammatory response

scholarly journals Expression and role of ABIN1 in sepsis: In vitro and in vivo studies

Open Medicine ◽  
2020 ◽  
Vol 16 (1) ◽  
pp. 033-040
Author(s):  
Haolan Li ◽  
Aichen Sun ◽  
Taocheng Meng ◽  
Yan Zhu
Keyword(s):  
Inflammatory Response ◽  
Molecular Mechanisms ◽  
Organ Injury ◽  
In Vivo Studies ◽  
Inflammatory Factors ◽  
Septic Mouse ◽  
Raw264.7 Macrophages ◽  
Tnf Α

AbstractIn this research, we attempted to explain the effect and the related molecular mechanisms of ABIN1 in lipopolysaccharide (LPS)-induced septic mice or RAW264.7 macrophages. LPS was adopted to treat RAW264.7 macrophages for 4 h, and the levels of inflammatory factors were assessed by ELISA. Besides, ABIN1 expression was measured by quantitative reverse transcription polymerase chain reaction. Apparently, LPS enhanced immunoreaction, suggested by increased expression of IL-1β, tumor necrosis factor (TNF)-α, and IL-6. ABIN1 levels were obviously reduced compared to the control. Furthermore, we evaluated the roles of ABIN1-plasmid in immunoreaction and nuclear factor-κB (NF-κB) pathway. We found that ABIN1-plasmid significantly reduced the expression of IL-1β, TNF-α, and IL-6 in LPS-treated cells and inhibited NF-κB pathway activation. Meanwhile, a septic mouse mode was conducted to validate the role of ABIN1 in inflammatory response and organ damage in vivo. These data suggested that ABIN1-plasmid significantly inhibited the secretion of inflammatory cytokines and Cr, BUN, AST, and ALT levels in the serum of LPS-stimulated mice compared to LPS + control-plasmid group, reflecting the relieved inflammation and organ injury. In summary, the present findings indicated that ABIN1 alleviated sepsis by repressing inflammatory response through NF-κB signaling pathway, emphasizing the potential value of ABIN1 as therapeutic strategy for sepsis.

scholarly journals MODERN TREATMENT METHODS OF THE LOCALIZED INFLAMMATORY RESPONSE IN ACUTE CEREBRAL ISCHEMIA

2020 ◽  
Vol 8 (1) ◽  
pp. 8-14
Author(s):  
V. S. Lychko
Keyword(s):  
Inflammatory Response ◽  
Blood Serum ◽  
Proinflammatory Cytokines ◽  
Plasma Levels ◽  
Inflammatory Factors ◽  
Course Of Disease ◽  
Acute Cerebral Ischemia ◽  
Tnf Α ◽  
Days Of Therapy ◽  
Anti Inflammatory

The article shows the results of a complex study of the leading index changes of the cytokine profile in patients with the brain infarction (BI) in the course of therapy with human cryopreserved cord blood serum (CCBS). Plasma levels of proinflammatory cytokines (interleukine-6 (IL-6), tumor necrosis factor-α (TNF-α)) as well as anti-inflammatory factors – IL-4, IL‑10 were tested in the blood serum of 350 patients in the mentioned medical condition on the 1st, 10th and 21st days of therapy. All patients were divided into 2 groups: the 1st one (n = 175) got undifferentiated therapy with the additional administration of acetylsalicylic acid (ASA); the 2nd one (n = 175) got the therapy of 1st group complemented by administration of 1 ml of CCBS within 10 days. Additionally there were 2 more clinical sub-groups distinguished by National Institutes of Health Stroke Scale (NIHSS) according to disease severity level: A group (n = 183) included patients in medium severity condition; B group (n = 167) comprised patients in critical condition. Plasma levels of IL-4, IL-6, IL-10 and TNF-α were specified by means of enzyme-linked immunosorbent analysis. Summing up the above-mentioned, it is certain that the imbalance in immune system functioning, represented by a simultaneous lytic level increase of both proinflammatory (IL-6, TNF-α) and anti-inflammatory (IL‑4, IL-10) cytokines, is observed shortly after the start of BI. Additional administration of CCBS in a therapeutic complex caused more considerable and more rapid stabilization of proinflammatory factor values, which were ultimately close to the control ones. This substantially influenced the course of disease and its prognosis. The research showed no accurate reduction in anti-inflammatory cytokines levels of ІL-4 and ІL-10 which indicated intensive localized inflammatory response even at the end of the acute period of disease. However, comparing the mentioned values with those of the patients who were not additionally treated with CCBS, lower value levels have to be acknowledged. It may be explained by a more efficient and incipient reduction of proinflammatory cytokines concentration in the course of disease, which in its turn results in normalization of ІL-4 and ІL-10 levels.

scholarly journals The interaction effect of aerobic exercise and vitamin D supplementation on inflammatory factors, anti-inflammatory proteins, and lung function in male smokers: a randomized controlled trial

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Leila Nikniaz ◽  
Morteza Ghojazadeh ◽  
Hooman Nateghian ◽  
Zeinab Nikniaz ◽  
Mahdieh Abbasalizad Farhangi ◽  
...  
Keyword(s):  
Vitamin D ◽  
Lung Function ◽  
Aerobic Exercise ◽  
Serum Levels ◽  
Vitamin D Supplementation ◽  
Inflammatory Factors ◽  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D ◽  
Tnf Α ◽  
Inflammatory Proteins

Abstract Background This study aimed to investigate the interaction effect of aerobic exercise and vitamin D supplementation on inflammation (TNF-α, IL-6, CC16, SP-D, and CC16/SP-D ratio) and lung function (FEV1, FVC, and FEV1/FVC ratio) in male smokers. Methods After applying inclusion criteria, a total of 40 healthy male smokers were recruited in this study. The participants were randomly divided into four groups as follows: Aerobic Exercise + vitamin D Supplementation (AE + VitD, n = 10), Aerobic Exercise (AE, n = 10), vitamin D Supplementation (VitD, n = 10), and Control (C, n = 10). The participants in the AE + VitD and AE groups performed aerobic exercise training (running) up to 50% of the maximum heart rate, three times a week for four weeks. Participants in AE + VitD and VitD groups received 6000 IU/w vitamin D3 for four weeks. The participants in control group did not receive any intervention. Serum tumor necrosis factor (TNF)-α, interleukin (IL)-6, Clara cell protein (CC16), surfactant protein (SP)-D, CC16/SP-D ratio, and lung function (FEV1, FVC, and FEV1/FVC ratio) were measured before and after four weeks of intervention. Results Serum levels of TNF-α, IL-6, and CC16 decreased significantly in AE + VitD, VitD, and AE groups after four weeks (P < 0.05). Serum SP-D level decreased significantly only in the AE + VitD group (P = 0.011). In addition, FEV1 and FVC increased significantly (P < 0.05) in AE + VitD and AE groups after four weeks of intervention. However, the interventions did not have a significant effect on CC16/SP-D ratio and FEV1/FVC ratio (P > 0.05). Furthermore, serum levels of 1,25-dihydroxyvitamin D increased significantly in AE + VitD and VitD groups (P < 0.05) after four weeks of intervention. However, except for TNF-α, between-group comparisons showed no significant differences in levels of IL-6, CC16, SP-D, CC16/SP-D ratio, FEV1, FVC, FEV1/FVC, and 1,25-dihydroxyvitamin D (P > 0.05). Conclusions The results of present study were that aerobic exercise combined with vitamin D supplementation can reduce serum inflammatory factors and anti-inflammatory proteins and improve lung function after four weeks of intervention. Further trials with larger sample size and longer duration are suggested to confirm these results. Trial registration Retrospectively registered. IRCT20180513039637N4. Registration date: 2020/10/20. URL: https://www.irct.ir/search/result?query=IRCT20180513039637N4

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