Relationship between serum IL10 level and p38MAPK enzyme activity on behavioral and cellular aspects of variation of hyperalgesia during different stages of arthritis in rats

Zaringhalam, Jalal; Akhtari, Zeinab; Eidi, Akram; Ruhani, Ali Haeri; Tekieh, Elaheh

doi:10.1007/s10787-013-0174-8

Cited by 20 publications

(10 citation statements)

References 19 publications

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“…TGF- β 1 played a key role in the progression of pulmonary fibrosis by promoting proliferation and differentiation of fibroblasts, enhancing synthesis of collagen, and altering some components in EMC [31]. Smad proteins are the main signal transducers for TGF- β 1 signaling pathway [32], in which Smad3 binds to Smad 4 to form a complex and then make an entry into the nucleus in order to regulate the targeted gene transcription, which thereby interfere with the formation of lung fibrosis [33]. On the contrary, Smad7 inhibits pulmonary fibrosis by competitively binding to TGF- β 1 and its receptors complex with Smad3 [34].…”

Section: Discussionmentioning

confidence: 99%

Yangyin Yiqi Mixture Ameliorates Bleomycin-Induced Pulmonary Fibrosis in Rats through Inhibiting TGF-β1/Smad Pathway and Epithelial to Mesenchymal Transition

Meng

Zhang

Wang

et al. 2019

Evidence-Based Complementary and Alternative Medicine

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Objective The aim of the current study was to investigate the protective effect of Yangyin Yiqi Mixture (YYYQ) on Bleomycin-induced pulmonary fibrosis in rats based on TGF-β1/Smad signal pathway and epithelial to mesenchymal transition (EMT). Methods 120 Wistar rats were randomly divided into six groups: control group, BLM group, BLM + Pred group, BLM+YYYQ-L group, BLM+YYYQ-M group, and BLM+YYYQ-H group. Rats were given an intratracheal instillation of 3 mg/kg BLM to establish the pulmonary fibrosis model and followed by different dosages of YYYQ (11, 22, 44g/kg, via intragastric gavage) or prednisone soluble (4.2mg/kg, via intragastric gavage) or water. After 14 days and 28 days, tissue sections were stained with hematoxylin-eosin and Masson's trichrome to observe histopathological changes. Protein levels of TGF-β1, CTGF, Interleukin 18, and hydroxyproline were detected by ELISA method, and mRNA expressions of TGF-β1, TβRI, TβRII, Smad3, Smad7, α-SMA, E-cadherin, laminin, and collagen I were detected by RT-PCR. Results TGF-β1, CTGF, Interleukin 18, and hydroxyproline levels and mRNA expression of TGF-β1, TβRI, TβRII, Smad3, α-SMA, laminin, and collagen I were significantly increased (p <0.01), while Smad7 and E-cadherin levels were significantly decreased in BLM group (p <0.01). YYYQ-M and YYYQ-H group had downregulated the TGF-β1, CTGF, hydroxyproline contents, and mRNA expression of TGF-β1, TβRI, TβRII, Smad3, α-SMA, laminin, and collagen I and upregulated mRNA levels of Smad7 and E-cadherin significantly (p <0.01 or p <0.05). The result from the present study, which was also supported by histological evidence, suggested that YYYQ-M group and YYYQ-H group exhibited better treatment effect on Bleomycin-induced pulmonary fibrotic rats when compared to that of BLM + Pred group (p <0.01). Meanwhile, the effect of YYYQ, in three different dosages, on the level of interleukin 18 was not significant. Conclusion These results showed that YYYQ has the potential of ameliorating the progression of pulmonary fibrosis, and the mechanism may be related to suppressing TGF-β1/Smad signal pathway and EMT in BLM-induced pulmonary fibrosis of rats.

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Section: Discussionmentioning

confidence: 99%

Yangyin Yiqi Mixture Ameliorates Bleomycin-Induced Pulmonary Fibrosis in Rats through Inhibiting TGF-β1/Smad Pathway and Epithelial to Mesenchymal Transition

Meng

Zhang

Wang

et al. 2019

Evidence-Based Complementary and Alternative Medicine

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“…In this study, considering our previous studies, the molecular parameters (spinal p38MAPK, Pp38MAPK, MOR and β-actin), behavioral test (hyperalgesia), and paw edema and serum IL-1β levels were assessed on days 0 (before CFA injection), 7 (inflammatory phase), 14, and 21 (arthritic phase) (Zaringhalam et al, 2014).…”

Section: Methodsmentioning

confidence: 99%

“…Activated p38MAPK (Phospho-p38MAPK) in the spinal cord is thought to play a key role in inflammation-induced spinal hyperalgesia, phosphorylation of transcription factors in the nucleus responsible for immediate-early genes regulation, provocation of other protein kinases, and mRNA stabilization (Zaringhalam, Akhtari, Eidi, Ruhani, & Tekieh, 2014). It seems that inhibition of proinflammatory cytokines like IL-1β and intracellular signaling pathways like p38MAPK could be a promising strategy to control inflammatory symptoms in RA (Korb et al, 2006; Moradi et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

Research Paper: The Effect of Orally Administered Probiotics on the Behavioral, Cellular, and Molecular Aspects of Adjuvant-Induced Arthritis

Shadnoush

Nazemian

Manaheji

et al. 2018

Basic Clin. Neurosci. J.

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Introduction:Rheumatoid Arthritis (RA) is a chronic autoimmune disease, which is accompanied with pain, hyperalgesia, and edema. Overproduction of pro-inflammatory cytokines and activation of intracellular signaling pathways sustain the RA symptoms considerably. There is a strong correlation between the expression of cytokines and opioid receptors in the arthritis process. Studies have shown that probiotics via different pathways such as reducing the levels of pro-inflammatory cytokines can alleviate inflammatory symptoms. Therefore, based on the crucial role of cellular and humoral immunity in induction of RA symptoms and potency of probiotics in modulation of immune responses, the purpose of this study was to investigate the effect of orally administered probiotics on the behavioral, cellular and molecular aspects of adjuvant-induced arthritis in male Wistar rats.Methods:Complete Freund’s Adjuvant (CFA)-induced arthritis was caused by single subcutaneous injection of CFA into the rat’s hind paw on day 0. Different doses of probiotics (1/250, 1/500 and 1/1000 [109 CFU/g]) were administered daily (gavage) after CFA injection. Hyperalgesia, edema, serum IL-1β levels, μ-Opioid Receptor (MOR) expression, and p38MAPK (Mitogen-Activated Protein Kinase) activities were assessed on days 0, 7, 14 and 21 of the study.Results:The results of this study indicated the efficacy of probiotics in reducing hyperalgesia, edema, serum levels of Interleukin-1β, and p38MAPK pathway activity during different phases of arthritis as well as increasing the expression of MORs during chronic phase of CFA-induced arthritis.Conclusion:It seems that probiotics can effectively reduce inflammatory symptoms by inhibiting the intracellular signaling pathway and cytokine production.

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“…Smad proteins were the main signal transducers of the TGF-β signaling pathway, in which Smad3 binds to Smad4, forms a complex and enters the nucleus to regulate the targeted gene transcription, which thereby interferes with the formation of lung fibrosis (Yamazaki et al, 2017). On the contrary, Smad7 inhibits pulmonary fibrosis by competitively binding to TGF-β and its receptors complex with Smad3 (Zaringhalam et al, 2014;Yan et al, 2016).…”

Section: Discussionmentioning

confidence: 99%

Effects of Nervilia fordii Extract on Pulmonary Fibrosis Through TGF-β/Smad Signaling Pathway

Yao

Yuan

et al. 2021

Front. Pharmacol.

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Idiopathic pulmonary fibrosis (IPF) is a progressive and irreversible interstitial pulmonary disease with a poor prognosis. The extract of Nervilia fordii (NFE) has shown remarkable benefit in the treatment of acute lung injury, lung cancer, and severe acute respiratory syndrome (SARS). However, the potential mechanism and efficacy of NFE in the treatment of IPF remain unknown. In this study, a systematic network pharmacology analysis was used to predict the mechanism and efficacy of NFE in the treatment of IPF, based on the major components of NFE elucidated by UPLC-TOF-MS/MS. The potential molecular interactions between the compounds and potential targets were predicted using molecular docking. In vivo, rats with pulmonary fibrosis induced by a single intratracheal injection of bleomycin (BLM) were orally administered NFE for 14 days. Lung index and biochemical levels were determined, and histopathological analysis using hematoxylin and eosin (H&E) and Masson staining was performed. The effects of NFE on fibroblast proliferation in Lipopolysaccharide (LPS) and TGF-β1-induced mouse 3T6 fibroblasts were evaluated in vitro. In total, 20 components were identified in NFE, and 102 potential targets for IPF treatment were predicted. These targets potentially participate in processes regulated by transmembrane receptor protein tyrosine kinase, ERBB2, and et al. Molecular docking results predicted high affinity interactions between three components (rhamnazin, rhamnetin, and rhamnocitrin) and the potential targets, suggesting that TGF-β is the most important potential target of NFE in the treatment of pulmonary fibrosis. NFE significantly decreased the lung index and alleviated BLM-induced pulmonary fibrosis in rats. Histopathological observation of lung tissues showed that NFE alleviated inflammation and collagen deposition in BLM-induced rats. NFE inhibited the migration of LPS- and TGF-β1-induced 3T6 fibroblasts, reduced the contents of hydroxyproline and collagen, and contributed to anti-inflammation and anti-oxidation. With the intervention of NFE, the protein and RNA expression of TGF-β1, a-SMA, Smad3/4, p-Smad3/4, CTGF, and p-ERK1/2 were significantly downregulated, while Smad7 and ERK1/2 were upregulated significantly in vivo and in vitro. These findings indicated that NFE may exert therapeutic effects on pulmonary fibrosis by alleviating inflammation, oxidation, and collagen deposition. The mechanism related to the inhibition of the TGF-β/Smad signaling pathway.

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Relationship between serum IL10 level and p38MAPK enzyme activity on behavioral and cellular aspects of variation of hyperalgesia during different stages of arthritis in rats

Cited by 20 publications

References 19 publications

Yangyin Yiqi Mixture Ameliorates Bleomycin-Induced Pulmonary Fibrosis in Rats through Inhibiting TGF-β1/Smad Pathway and Epithelial to Mesenchymal Transition

Yangyin Yiqi Mixture Ameliorates Bleomycin-Induced Pulmonary Fibrosis in Rats through Inhibiting TGF-β1/Smad Pathway and Epithelial to Mesenchymal Transition

Research Paper: The Effect of Orally Administered Probiotics on the Behavioral, Cellular, and Molecular Aspects of Adjuvant-Induced Arthritis

Effects of Nervilia fordii Extract on Pulmonary Fibrosis Through TGF-β/Smad Signaling Pathway

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