The Experts below are selected from a list of 588 Experts worldwide ranked by ideXlab platform
Yuehling Hsieh - One of the best experts on this subject based on the ideXlab platform.
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the effects of laser acupuncture on the modulation of cartilage extracellular matrix macromolecules in rats with adjuvant induced arthritis
PLOS ONE, 2019Co-Authors: Tienchien Pan, Yuhsin Tsai, Wen Chi Chen, Yuehling HsiehAbstract:OBJECTIVES Articular cartilage damage related to irreversible physical disability affects most patients with chronic rheumatoid arthritis (RA). Strategies targeting the preservation of cartilage function are needed. Laser acupuncture (LA) can be an emerging alternative therapy for RA; however, its molecular mechanism underlying the beneficial effect on cartilage has not been elucidated. This study aimed to examine the potential chondroprotective effects of LA on extracellular matrix (ECM) macromolecules and proinflammatory cytokines in the articular cartilage of adjuvant-induced arthritis (AIA) rats and explore its related mechanisms. DESIGN Monoarthritis was induced in adult male Sprague-Dawley rats (250-300 g) via intraarticular injection of complete Freund's adjuvant (CFA) into the Tibiotarsal Joint. Animals were treated with LA at BL60 and KI3 acupoints three days after CFA administration with a 780 nm GaAlAs laser at 15 J/cm2 daily for ten days. The main outcome measures including paw circumference, paw withdrawal threshold, histopathology and immunoassays of tumor necrosis factor-α (TNF-α), collagen type II (CoII), cartilage oligomeric matrix protein (COMP) were analyzed. RESULTS LA significantly reduced ankle edema and inflammation-induced hyperalgesia in AIA rats (P < 0.05). Moreover, the TNF-α levels were significantly decreased while CoII, COMP and proteoglycans proteins were significantly enhanced following LA stimulation of the AIA cartilage compared to those treated with sham-LA (P < 0.05). CONCLUSIONS LA attenuates cartilage degradation in AIA rat by suppressing TNF-α activation and up-regulating ECM macromolecules, suggesting LA might be of potential clinical interest in RA treatment.
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hyaluronan modulates accumulation of hypoxia inducible factor 1 alpha inducible nitric oxide synthase and matrix metalloproteinase 3 in the synovium of rat adjuvant induced arthritis model
Arthritis Research & Therapy, 2011Co-Authors: John Wang, Liwei Chou, Peilin Chang, Yuehling HsiehAbstract:Hypoxia is a feature of the inflamed synovium in rheumatoid arthritis (RA). Intra-articular injection of hyaluronan (HA) may be considered a potential way to treat RA. However, the exact molecular mechanism of HA on decreased cellular responses to hypoxic environment is unclear. The present study has been designed to use the adjuvant-induced arthritis model to examine the effects of HA on the changes of immunohistochemical expressions of hypoxia-inducible factor-1alpha (HIF-1alpha), inducible nitric oxide synthase (iNOS), and matrix metalloproteinase-3 (MMP3) in the synovial tissues at the early phase of arthritic inflammation. Monoarthritis was induced in adult male Sprague-Dawley (250-300 g) via intraarticular injection of complete Freund's adjuvant (CFA) into the Tibiotarsal Joint. The CFA-induction arthritis animals were divided into three groups: treatment (intraarticular injection of HA), placebo (intraarticular injection of saline) and controls (no treatments). Functional evaluations of edema and pain behavior, histology, and HIF-1alpha, iNOS, and MMP3 immunohistochemistry were performed before, after the first injection, three injections, and on the follow-up injection of the treatments. Intra-articular injection of HA also significantly suppressed the mechanical allodynia (p < 0.001) and overexpressions of HIF-1alpha (p < 0.001), iNOS (p = 0.004) and MMP3 (p < 0.001) immunoreactivity in synovium. This study demonstrated that early intervention of HA is an effective protection against accumulation of inflammation-induced HIF-1alpha, iNOS, and MMP3 to limit erosive damage in CFA-induced model of arthritis.
Liwei Chou - One of the best experts on this subject based on the ideXlab platform.
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hyaluronan modulates accumulation of hypoxia inducible factor 1 alpha inducible nitric oxide synthase and matrix metalloproteinase 3 in the synovium of rat adjuvant induced arthritis model
Arthritis Research & Therapy, 2011Co-Authors: John Wang, Liwei Chou, Peilin Chang, Yuehling HsiehAbstract:Hypoxia is a feature of the inflamed synovium in rheumatoid arthritis (RA). Intra-articular injection of hyaluronan (HA) may be considered a potential way to treat RA. However, the exact molecular mechanism of HA on decreased cellular responses to hypoxic environment is unclear. The present study has been designed to use the adjuvant-induced arthritis model to examine the effects of HA on the changes of immunohistochemical expressions of hypoxia-inducible factor-1alpha (HIF-1alpha), inducible nitric oxide synthase (iNOS), and matrix metalloproteinase-3 (MMP3) in the synovial tissues at the early phase of arthritic inflammation. Monoarthritis was induced in adult male Sprague-Dawley (250-300 g) via intraarticular injection of complete Freund's adjuvant (CFA) into the Tibiotarsal Joint. The CFA-induction arthritis animals were divided into three groups: treatment (intraarticular injection of HA), placebo (intraarticular injection of saline) and controls (no treatments). Functional evaluations of edema and pain behavior, histology, and HIF-1alpha, iNOS, and MMP3 immunohistochemistry were performed before, after the first injection, three injections, and on the follow-up injection of the treatments. Intra-articular injection of HA also significantly suppressed the mechanical allodynia (p < 0.001) and overexpressions of HIF-1alpha (p < 0.001), iNOS (p = 0.004) and MMP3 (p < 0.001) immunoreactivity in synovium. This study demonstrated that early intervention of HA is an effective protection against accumulation of inflammation-induced HIF-1alpha, iNOS, and MMP3 to limit erosive damage in CFA-induced model of arthritis.
Lucy F Donaldson - One of the best experts on this subject based on the ideXlab platform.
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characterisation of a freund s complete adjuvant induced model of chronic arthritis in mice
Journal of Neuroscience Methods, 2003Co-Authors: Naomi L Chillingworth, Lucy F DonaldsonAbstract:Abstract Freund's complete adjuvant (FCA)-induced arthritis is a commonly used model in the rat. Use of FCA to induce arthritis in mice has been only occasionally reported, and most attempts to use this model have met with little success. Subdermal injection of FCA at multiple sites around the Tibiotarsal Joint of male C57Bl6 mice caused a localised inflammatory reaction to develop in 24 h. Significant swelling occurred around the injected Tibiotarsal Joint within 24 h ( P P P
Achille P Caputi - One of the best experts on this subject based on the ideXlab platform.
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cloricromene a coumarine derivative protects against collagen induced arthritis in lewis rats
British Journal of Pharmacology, 2000Co-Authors: Salvatore Cuzzocrea, Emanuela Mazzon, Carla Bevilaqua, Giuseppina Costantino, Domenico Britti, G Mazzullo, Angela De Sarro, Achille P CaputiAbstract:The aim of the present study was to investigate the effects of cloricromene, a coumarine derivative, in rats subjected to collagen-induced arthritis. Collagen-induced arthritis (CIA) was induced in Lewis rats by an intradermal injection of 100 μl of the emulsion (containing 100 μg of bovine type II collagen) (CII) and complete Freund's adjuvant (CFA) at the base of the tail. On day 21, a second injection of CII in CFA was administered. Lewis rats developed an erosive hind paw arthritis when immunized with CII in CFA. Macroscopic clinical evidence of CIA first appeared as peri-articular erythema and oedema in the hind paws. The incidence of CIA was 100% by day 27 in the CII challenged rats and the severity of CIA progressed over a 35-day period with radiographic evaluation revealing focal resorption of bone together with osteophyte formation in the Tibiotarsal Joint and soft tissue swelling. The histopathology of CIA included erosion of the cartilage at the Joint margins. Treatment of rats with cloricromene (10 mg kg−1 i.p. daily) starting at the onset of arthritis (day 23), delayed the development of the clinical signs at days 24–35 and improved histological status in the knee and paw. Immunohistochemical analysis for iNOS, COX-2, nitrotyrosine and for poly (ADP-ribose) synthetase (PARS) revealed a positive staining in inflamed Joints from collagen-treated rats. The degree of staining for iNOS, COX-2, nitrotyrosine and PARS were markedly reduced in tissue sections obtained from collagen-treated rats, which had received cloricromene. Radiographic signs of protection against bone resorption and osteophyte formation were present in the Joints of cloricromene-treated rat. This study provides the first evidence that cloricromene, a coumarine derivative, attenuates the degree of chronic inflammation and tissue damage associated with collagen-induced arthritis in the rat. British Journal of Pharmacology (2000) 131, 1399–1407; doi:10.1038/sj.bjp.0703695
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beneficial effects of tempol a membrane permeable radical scavenger in a rodent model of collagen induced arthritis
Arthritis & Rheumatism, 2000Co-Authors: Salvatore Cuzzocrea, Emanuela Mazzon, Giuseppina Costantino, Domenico Britti, G Mazzullo, Achille P Caputi, Michelle C Mcdonald, Helder Motafilipe, Christoph ThiemermannAbstract:Objective To investigate the effects of tempol, a membrane-permeable radical scavenger, in rats with collagen-induced arthritis (CIA). Methods CIA was induced in Lewis rats by intradermal injection of 100 μl of an emulsion of 100 μg of bovine type II collagen (CII) in complete Freund's adjuvant (FCA) at the base of the tail. On day 21, a second injection of CII in FCA was administered. Results Lewis rats developed an erosive arthritis of the hind paws when immunized with CII in FCA. Macroscopic evidence of CIA first appeared as periarticular erythema and edema in the hind paws. The incidence of CIA was 100% by day 27 in the CII-challenged rats, and the severity of CIA progressed over a 35-day period. Radiographs revealed focal resorption of bone, with osteophyte formation in the Tibiotarsal Joint, and soft tissue swelling. The histopathologic features included erosion of the cartilage at the Joint margins. Treatment of rats with tempol (10 mg/kg/day intraperitoneally) starting at the onset of arthritis (day 23) delayed the development of the clinical signs on days 24–35 and improved the histologic status of the knee and paw. Immunohistochemical analysis for nitrotyrosine and poly(ADP-ribose) synthetase (PARS) revealed positive staining in the inflamed Joints of CII-treated rats. The degree of nitrotyrosine and PARS staining was markedly reduced in tissue sections obtained from CII-treated rats that had received tempol. Furthermore, radiographs revealed protection against bone resorption and osteophyte formation in the Joints of tempol-treated rats. Conclusion This study is the first to provide evidence that tempol, a small molecule that permeates biologic membranes and scavenges reactive oxygen species, attenuates the degree of chronic inflammation and tissue damage associated with CIA in the rat.
Tania F. Salvini - One of the best experts on this subject based on the ideXlab platform.
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insulin treatment reverses the increase in atrogin 1 expression in atrophied skeletal muscles of diabetic rats with acute Joint inflammation
Therapeutics and Clinical Risk Management, 2018Co-Authors: Clara Maria Pinheirodardis, Joao Luiz Quagliotti Durigan, Tania F. Salvini, Sabrina Messa Peviani, Vânia Ortega Gutierres, Renata Pires Assis, Gabriel Borges Delfino, Amanda Martins Baviera, Iguatemy Lourenco BrunettiAbstract:Background The aim of this study was to evaluate the changes in biomarkers of skeletal muscle proteolysis (atrogin-1, muscle RING finger-1 protein [MuRF-1]) and inflammation (nuclear factor kappa-B) in skeletal muscles of rats under two catabolic conditions, diabetes mellitus (DM) and acute Joint inflammation, and the effects of insulin therapy. Materials and methods Male Wistar rats were divided into groups without diabetes - normal (N), saline (NS), or ι-carrageenan (NCa) injection into the Tibiotarsal Joint - and groups with diabetes - diabetes (D), plus insulin (DI), saline (DS), or ι-carrageenan (DCa) injection into the Tibiotarsal Joint, or ι-carrageenan injection and treatment with insulin (DCaI). Three days after ι-carrageenan injection (17 days after diabetes induction), tibialis anterior (TA) and soleus (SO) skeletal muscles were used for analysis. Results DM alone caused a significant decrease in the mass of TA and SO muscles, even with low levels of atrogenes (atrogin-1, MuRF-1), which could be interpreted as an adaptive mechanism to spare muscle proteins under this catabolic condition. The loss of muscle mass was exacerbated when ι-carrageenan was administered in the Joints of diabetic rats, in association with increased expression of atrogin-1, MuRF-1, and nuclear factor kappa-B. Treatment with insulin prevented the increase in atrogin-1 (TA, SO) and the loss of muscle mass (SO) in diabetic-carrageenan rats; in comparison with TA, SO muscle was more responsive to the anabolic actions of insulin. Conclusion Acute Joint inflammation overcame the adaptive mechanism in diabetic rats to prevent excessive loss of muscle mass, worsening the catabolic state. The treatment of diabetic-carrageenan rats with insulin prevented the loss of skeletal muscle mass mainly via atrogin-1 inhibition. Under the condition of DM and inflammation, muscles with the prevalence of slow-twitch, type 1 fibers were more responsive to insulin treatment, recovering the ability to grow.
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Effect of Tibiotarsal Joint inflammation on gene expression and cross-sectional area in rat soleus muscle
2016Co-Authors: Carolina Ramirez, Thiago Luiz Russo, Sabrina Messa Peviani, Gabriel Delfino, Carolina Alcântara, Tania F. SalviniAbstract:ABSTRACT | Background: Joint inflammation is a common clinical problem in patients treated by physical therapists. The hypothesis of this study is that Joint inflammation induces molecular and structural changes in the soleus muscle, which is composed mainly of slow-twitch muscle fibers. Objective: To study the effect of Tibiotarsal Joint inflammation on muscle fiber cross-sectional area (CSA), gene expression levels (atrogin-1, MuRF1, MyoD, myostatin, p38MAPK, NFκB, TNF-alpha), and TNF-alpha protein in the soleus muscle. Method: Wistar rats were randomly divided into 3 periods (2, 7 and 15 days) and assigned to 4 groups (control, sham, inflammation, and immobilization). Results: In the inflammation group at 2 days, MuRF1 and p38MAPK expression had increased, and NFκB mRNA levels had decreased. At 7 days, myostatin expression had decreased. At 7 and 15 days, this group had muscle fiber CSA reduction. At 2 days, the immobilization group showed increased atrogin-1, MuRF1, NFκB, MyoD, and p38MAPK expressions and reduced muscle fiber CSA. At 7 and 15 days, myostatin mRNA levels had increased, and the CSA had decreased. The sham group showed increased p38MAPK and myostatin expressions at 2 and 7 days, respectively. No changes occurred in TNF-alpha gene or protein expression. Conclusion: Acute Joint inflammation induces gene expression related to the proteolytic pathway without reduction in muscle fiber CSA. Chronic Joint inflammation induced muscle atrophy without up-regulation of important genes belonging to the proteolytic pathway. Thus, muscle adaptation may differ according to the stage of Joint inflammation, which suggests that the therapeutic modalities used by physical therapists at eac
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Joint inflammation alters gene and protein expression and leads to atrophy in the tibialis anterior muscle in rats
American Journal of Physical Medicine & Rehabilitation, 2011Co-Authors: Carolina Ramirez, Thiago Luiz Russo, Maria Cristina Sandoval, Adriana Abbade Dentillo, Marcela Abreu Silva Couto, Joao Luiz Quagliotti Durigan, Tania F. SalviniAbstract:Ramirez C, Russo TL, Sandoval MC, Dentillo AA, Couto MAS, Durigan JLQ, Salvini TF: Joint inflammation alters gene and protein expression and leads to atrophy in the tibialis anterior muscle in rats. Am J Phys Med Rehabil 2011;90:930Y939. Objective: The aim of this study was to evaluate the effect of Tibiotarsal Joint inflammation in rat tibialis anterior muscle through muscle fiber cross-sectional area (CSA) and gene expression (atrogin-1, muscle ring fingerY 1[ MuRF1], myogenic differentiation-1 [MyoD], p38 mitogen-activated protein kinase [p38MAPK], nuclear factor kappa BYdependent [NFJB], tumor necrosis factorYalpha [TNF->]). Design: Wistar rats were randomly divided into three periods (2, 7, and 15 days) and assigned into four groups within each experimental period: control, sham, inflammation, and immobilization. Real-time polymerase chain reaction, Western blot, immunofluorescence, and muscle fiber CSA analyses were performed. Results: At 2 days, the inflammation group increased atrogin-1, MuRF1, and myostatin and reduced MyoD expression. At 7 days, the inflammation group increased atrogin-1, MuRF1, NFJB, p38MAPK, MyoD, myostatin, and TNF-> expression and TNF-> protein and reduced muscle fiber CSA. At 15 days, gene and protein expression in the inflammation group returned to basal levels, and CSA values were similar to those in control and sham groups. The immobilization groups have a similar pattern in all experimental periods, with increased atrogin-1, MuRF1, NFJB, and TNF-> gene expression and reduced muscle fiber CSA. The sham group had increased myostatin and atrogin-1 expression at 2 days and increased MyoD and myostatin expression at 7 days.