Background Achilles tendinopathy, a common cause of heel pain, is primarily considered mechanical in origin, but its pathogenesis and treatment lack consensus. Molecules such as collagen peptide type-1, low molecular weight chondroitin sulphate, sodium hyaluronate and vitamin C have been shown to act as building blocks of tendon structure, and oral supplementation of these have promising results in Achilles tendinopathy. Methods This study was a prospective randomized control trial to compare the effectiveness of oral diclofenac sodium versus a nutraceutical combination of collagen peptide type-1, chondroitin sulphate, sodium hyaluronate, and vitamin C in the treatment of Achilles tendinopathy on pain and ultrasonographic structures. A total of 40 patients satisfying inclusion and exclusion criteria were randomly allocated into two groups and were given the nutraceutical combination in group A and diclofenac sodium in group B. The patient evaluation was done at baseline, six-week, and 12-week intervals in terms of VAS (Visual Analogue Scale) and tendo-Achilles thickness by ultrasound. Results Both nutraceutical combination and diclofenac reduced pain in persons with Achilles tendinopathy. The nutraceutical combination had a statistically significant better outcome in reducing pain at the end of 12 weeks. On ultrasound, both the interventions reduced Achilles tendon anteroposterior and mediolateral thickness by the end of 12 weeks. Although there was no absolute significant intergroup difference, the percentage change was more in the nutraceutical group in the case of anteroposterior thickness. Conclusion Combining collagen peptide type-1, low molecular weight chondroitin sulphate, sodium hyaluronate, and vitamin C is more effective than oral diclofenac in controlling pain in Achilles tendinopathy.
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http://dx.doi.org/10.7759/cureus.19737 | DOI Listing |
Sci Rep
December 2024
Clinical Laboratory, Hebei General Hospital, Shijiazhuang, Hebei, China.
Objective: To explore the influence of SALL4 in cardiac fibroblasts on the progression of myocardial infarction.
Methods: Analysis of genes specifically expressed in myocardial infarction by bioinformatics methods; The impact of SALL4 on myocardial infarction was assessed using mouse ultrasound experiments and Masson staining; The effect of SALL4 on the expression levels of collagen-I and collagen-III in myocardial tissue was examined by immunohistochemical staining; The migration ability of cardiac fibroblasts was evaluated using a Transwell assay; The proliferative ability of cardiac fibroblasts was tested using a CCK-8 assay; The relative fluorescence intensity of α-SMA and CTGF in cardiac fibroblasts were checked through immunofluorescence staining experiment; The expression of SALL4, DOT1L, H3K79me2, P53, SHP2, YAP, nucleus-YAP, collagen-I, α-SMA, CTGF, and PAI-1 in myocardial tissues or cardiac fibroblasts was detected using western blot analysis.
Results: SALL4-specific high expression in myocardial infarction; SALL4 intensified the alterations in the heart structure of mice with myocardial infarction and worsened the fibrosis of myocardial infarction; SALL4 also promoted the expression of SALL4, DOT1L, H3K79me2, P53, SHP2, YAP, nucleus-YAP, collagen-I, collagen-III, α-SMA, CTGF, and PAI-1 in myocardial infarction tissues and cardiac fibroblasts; Subsequently, SALL4 could enhance the immunofluorescence intensity of α-SMA and CTGF; Moreover, SALL4 could promote the proliferation and migration of cardiac fibroblasts.
Sci Rep
December 2024
Department of Pharmacy, The Second Affiliated Hospital of Dalian Medical University, #467 Zhongshan Road, Dalian, 116023, Liaoning, China.
Sodium-glucose co-transport protein 2 (SGLT2) inhibitors, a novel category of oral hypoglycemic agents, offer a promising outlook for individuals experiencing heart failure with reduced ejection fraction. Evidence is emerging that highlights their potential in alleviating myocardial fibrosis and oxidative stress. However, the precise mechanisms through which SGLT2 inhibitors influence myocardial fibrosis induced by angiotensin II (Ang II) or transforming growth factor-β1 (TGF-β1) are not fully understood.
View Article and Find Full Text PDFJOR Spine
December 2024
Trinity Centre for Biomedical Engineering Trinity Biomedical Sciences Institute, Trinity College Dublin, The University of Dublin Dublin Ireland.
Background: Low back pain (LBP) is predominantly caused by degeneration of the intervertebral disc (IVD) and central nucleus pulposus (NP) region. Conservative treatments fail to restore disc function, motivating the exploration of nucleic acid therapies, such as the use of microRNAs (miRNAs). miRNAs have the potential to modulate expression of discogenic factors, while silencing the catabolic cascade associated with degeneration.
View Article and Find Full Text PDFFront Immunol
December 2024
Coagulation Laboratory, Department of Laboratory Medicine, Ghent University Hospital, Ghent, Belgium.
Introduction: Unfolded Von Willebrand Factor (VWF) is increased in thrombotic pathologies such as myocardial infarction. Unfolded VWF mediates the binding of platelets without the need for collagen. β-glycoprotein I (β-GPI) is a natural inhibitor of the platelet-VWF interaction.
View Article and Find Full Text PDFNan Fang Yi Ke Da Xue Xue Bao
December 2024
Department of Laboratory Medicine, Hengyang First People's Hospital, Hengyang 421001, China.
Objectives: To investigate the protective effect of the probiotic bacterium K12 (K12) against (Mp) infection in mice.
Methods: Forty male BALB/c mice were randomized into normal control group, K12 treatment group, Mp infection group, and K12 pretreatment prior to Mp infection group. The probiotic K12 was administered daily by gavage for 14 days before Mp infection induced by intranasal instillation of Mp.
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