High intensity interval training is superior to moderate intensity continuous training in enhancing the anti-inflammatory and apoptotic effect of pentoxifylline in the rat model of endometriosis
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High intensity interval training enhanced pentoxifylline's anti-inflammatory and apoptotic effects in a rat model of endometriosis more than moderate intensity continuous training.
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Abstract
This study investigated the effects of pentoxifylline (PTX), high intensity interval training (HIIT) and moderate intensity continuous training (MICT) separately and in combination, on inflammatory and apoptotic pathways in the rat model of induced endometriosis. Endometriosis was induced through surgery on female Sprague-Dawley rats. Six weeks after the first surgery, the second look laparotomy was performed. After induction of endometriosis in rats, they were divided into control, MICT, PTX, MICT+ PTX, HIIT, HIIT+PTX groups. Two weeks after the second look laparotomy, PTX and exercise training interventions were performed for eight weeks. Endometriosis lesions were assessed histologically. Proteins content of the NF-κB, PCNA and Bcl-2 were measured by immunoblotting and genes expression of the TNF-α and VEGF were measured by Real-time PCR methods. Findings of the study indicated that, PTX significantly decreased volume and histological grading of lesions, proteins of NF-κB and Bcl-2; and genes expression of the TNF-α, and VEGF in lesions. HIIT significantly decreased volume and histological grading of lesions, NF-κB, TNF-α and VEGF in lesions. MICT did not induce any significant effect on the study variables. Although, MICT+PTX decreased significantly volume and histological grading of lesions, as well as NF-κB, and Bcl-2 in lesions, however, these factors were not significantly different with the PTX group. HIIT+PTX decreased significantly all of the study variables compared to other interventions, except for VEGF when compared to PTX. In summary, combination of PTX and HIIT can induce enhancing effect on suppression of endometriosis through suppressing inflammation, angiogenesis, and proliferation and enhancing apoptosis.
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References (100)
- Agents Blocking the Nuclear Factor-κB Pathway Are Effective Inhibitors of Endometriosis in an in vivo Experimental Model via openalex
- Antiangiogenesis Therapy of Endometriosis Using PAMAM as a Gene Vector in a Noninvasive Animal Model via openalex
- An Update on the Multifaceted Role of NF-kappaB in Endometriosis via openalex
- Apoptosis and expression of Bcl-2 and Bax in eutopic endometrium from women with endometriosis via openalex
- Crocin improves endometriosis by inhibiting cell proliferation and the release of inflammatory factors via openalex
- Curcumin Attenuates TNF‐α‐induced Expression of Intercellular Adhesion Molecule‐1, Vascular Cell Adhesion Molecule‐1 and Proinflammatory Cytokines in Human Endometriotic Stromal Cells via openalex
- Cytokines, Angiogenesis, and Extracellular Matrix Degradation are Augmented by Oxidative Stress in Endometriosis via openalex
- Decrease in interferon gamma production and impairment of T-lymphocyte proliferation in peritoneal fluid of women with endometriosis via openalex
- Dual inhibition of ERK1/2 and AKT pathways is required to suppress the growth and survival of endometriotic cells and lesions via openalex
- Effect of Physical Exercise on Endometriosis Experimentally Induced in Rats via openalex
- Effect of Vascular Endothelial Growth Factor Inhibition on Endometrial Implant Development in a Murine Model of Endometriosis via openalex
- Endometriosis via openalex
- Endometriosis and physical exercises: a systematic review via openalex
- Endometriosis: An Inflammatory Disease That Requires New Therapeutic Options via openalex
- Hepatocyte nuclear factor-1 beta protects endometriotic cells against apoptotic cell death by up-regulating the expression of antiapoptotic genes† via openalex
- Immunolocalization of the apoptosis regulating proteins Bcl-2 and Bax in human endometrium and isolated peritoneal fluid macrophages in endometriosis via openalex
- Increased interleukin-6 levels in peritoneal fluid of infertile patients with active endometriosis via openalex
- Inflammatory Mediators and Pain in Endometriosis: A Systematic Review via openalex
- Lipopolysaccharide-promoted proliferation of endometriotic stromal cells via induction of tumor necrosis factor α and interleukin-8 expression via openalex
- Nuclear factor-kappa B is constitutively activated in peritoneal endometriosis via openalex
- Nuclear factor-kappa B signaling in endometriotic stromal cells is not inhibited by progesterone owing to an aberrant endoplasmic reticulum stress response: a possible role for an altered inflammatory process in endometriosis via openalex
- Overexpressed MPS-1 contributes to endometrioma development through the NF-κB signaling pathway via openalex
- Pathogenesis and pathophysiology of endometriosis via openalex
- Pathogenesis of Endometriosis: New Insights into Prospective Therapies via openalex
- Pathogenetic Significance of Increased Levels of Interleukin-8 in the Peritoneal Fluid of Patients with Endometriosis via openalex
- Pentoxifylline for the treatment of endometriosis-associated pain and infertility via openalex
- Peroxisome proliferator-activated receptor-γ ligand reduced tumor necrosis factor-α-induced interleukin-8 production and growth in endometriotic stromal cells via openalex
- Reduction of the intraperitoneal inflammation associated with endometriosis by treatment with medroxyprogesterone acetate via openalex
- Regulation of Matrix Metalloproteinase-2 Activity by COX-2-PGE2-pAKT Axis Promotes Angiogenesis in Endometriosis via openalex
- Resveratrol successfully treats experimental endometriosis through modulation of oxidative stress and lipid peroxidation via openalex
- Retraction: Ginsenoside Rf alleviates dysmenorrhea and inflammation through the BDNF-TrkB-CREB pathway in a rat model of endometriosis via openalex
- Surgical Removal of Endometrioma Decreases the NF-kB1 (p50/105) and NF-kB p65 (Rel A) Expression in the Eutopic Endometrium During the Implantation Window via openalex
- The effectiveness of Rutin for prevention of surgical induced endometriosis development in a rat model via openalex
- The Methyl Ester of 2-Cyano-3,12-Dioxooleana-1,9-Dien-28-Oic Acid Reduces Endometrial Lesions Development by Modulating the NFkB and Nrf2 Pathways via openalex
- The role of inflammation, oxidative stress, angiogenesis, and apoptosis in the pathophysiology of endometriosis: Basic science and new insights based on gene expression via openalex
- The role of NF-kappaB in endometriosis via openalex
- The stimulus responsible for the peritoneal fluid inflammation observed in infertile women with endometriosis via openalex
- Tumor Necrosis Factor-α-Induced Interleukin-8 (IL-8) Expression in Endometriotic Stromal Cells, Probably through Nuclear Factor-κB Activation: Gonadotropin-Releasing Hormone Agonist Treatment Reduced IL-8 Expression via openalex
- Tumor necrosis factor-α induced the release of interleukin-6 from endometriotic stromal cells by the nuclear factor-κB and mitogen-activated protein kinase pathways via openalex
- W3112681498 via openalex
- W3120501543 via openalex
- W3156626608 via openalex
- W3171821017 via openalex
- W4225146312 via openalex
- W4234160457 via openalex
- W4250344409 via openalex
- W4280609525 via openalex
- W4292550299 via openalex
- W4293247451 via openalex
- W4303627886 via openalex
- W6611762018 via openalex
- W6631841586 via openalex
- W6666217457 via openalex
- W6714341644 via openalex
- W6717046087 via openalex
- W6787372331 via openalex
- W6788961964 via openalex
- W6800736459 via openalex
- W6809451424 via openalex
- W6838279845 via openalex
- W1166858611 via openalex
- W6845525417 via openalex
- W1531751498 via openalex
- W1971586374 via openalex
- W1983684960 via openalex
- W2005764181 via openalex
- W2015065898 via openalex
- W2021345772 via openalex
- W2031811366 via openalex
- W2060627937 via openalex
- W2072591613 via openalex
- W2077575210 via openalex
- W2107713440 via openalex
- W2121836743 via openalex
- W2132695791 via openalex
- W2140906896 via openalex
- W2166781237 via openalex
- W2167318005 via openalex
- W2178698264 via openalex
- W2279472280 via openalex
- W2304378409 via openalex
- W2315613727 via openalex
- W2346020725 via openalex
- W2410194753 via openalex
- W2418550189 via openalex
- W2560768038 via openalex
- W2565571317 via openalex
- W2736643621 via openalex
- W2743517453 via openalex
- W2799744365 via openalex
- W2805545878 via openalex
- W2915178508 via openalex
- W2916807271 via openalex
- W2978644324 via openalex
- W2980504997 via openalex
- W2999837121 via openalex
- W3033392766 via openalex
- W3038076383 via openalex
- W3045375361 via openalex
- W3111112723 via openalex
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