Apocynin inhibits the upregulation of TGF-β1 expression and ROS production induced by TGF-β in skeletal muscle cells

Ábrigo, Johanna; Morales, María Gabriela; Simón, Felipe; Cabrera, Daniel; Capua, Gabriella Di; Cabello-Verrugio, Claudio

doi:10.1016/j.phymed.2015.06.011

Cited by 14 publications

(13 citation statements)

References 39 publications

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“…It has mostly been used as an inhibitor of NADPH oxidase activity [20, 21, 82, 85]. In this study, NADPH oxidase activity and AGEs did not differ between groups.…”

Section: Discussionmentioning

confidence: 45%

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Apocynin influence on oxidative stress and cardiac remodeling of spontaneously hypertensive rats with diabetes mellitus

Rosa¹,

Gimenes²,

Campos³

et al. 2016

Cardiovasc Diabetol

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PurposeAlthough increased oxidative stress is a major component of diabetic hypertensive cardiomyopathy, research into the effects of antioxidants on cardiac remodeling remains scarce. The actions of antioxidant apocynin include inhibiting reactive oxygen species (ROS) generation by nicotinamide adenine dinucleotide phosphate (NADPH) oxidases and ROS scavenging. We evaluated the effects of apocynin on cardiac remodeling in spontaneously hypertensive rats (SHR) with diabetes mellitus (DM).MethodsMale SHR were divided into four groups: control (SHR, n = 16); SHR treated with apocynin (SHR-APO; 16 mg/kg/day, added to drinking water; n = 16); diabetic SHR (SHR-DM, n = 13); and SHR-DM treated with apocynin (SHR-DM-APO, n = 14), for eight weeks. DM was induced by streptozotocin (40 mg/kg, single dose). Statistical analyzes: ANOVA and Tukey or Mann–Whitney.ResultsEchocardiogram in diabetic groups showed higher left ventricular and left atrium diameters indexed for body weight, and higher isovolumetric relaxation time than normoglycemic rats; systolic function did not differ between groups. Isolated papillary muscle showed impaired contractile and relaxation function in diabetic groups. Developed tension was lower in SHR-APO than SHR. Myocardial hydroxyproline concentration was higher in SHR-DM than SHR, interstitial collagen fraction was higher in SHR-DM-APO than SHR-APO, and type III collagen protein expression was lower in SHR-DM and SHR-DM-APO than their controls. Type I collagen and lysyl oxidase expression did not differ between groups. Apocynin did not change collagen tissue. Myocardial lipid hydroperoxide concentration was higher in SHR-DM than SHR and SHR-DM-APO. Glutathione peroxidase activity was lower and catalase higher in SHR-DM than SHR. Apocynin attenuated antioxidant enzyme activity changes in SHR-DM-APO. Advanced glycation end-products and NADPH oxidase activity did not differ between groups.ConclusionApocynin reduces oxidative stress independently of NADPH oxidase activity and does not change ventricular or myocardial function in spontaneously hypertensive rats with diabetes mellitus. The apocynin-induced myocardial functional impairment in SHR shows that apocynin actions need to be clarified during sustained chronic pressure overload.

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“…It has mostly been used as an inhibitor of NADPH oxidase activity [20, 21, 82, 85]. In this study, NADPH oxidase activity and AGEs did not differ between groups.…”

Section: Discussionmentioning

confidence: 45%

“…Apocynin can be isolated and purified from several plant species such as Picrorhiza kurroa , and has been evaluated in experimental studies as an anti-oxidant agent [82–84]. It has mostly been used as an inhibitor of NADPH oxidase activity [20, 21, 82, 85].…”

Section: Discussionmentioning

confidence: 99%

Apocynin influence on oxidative stress and cardiac remodeling of spontaneously hypertensive rats with diabetes mellitus

Rosa¹,

Gimenes²,

Campos³

et al. 2016

Cardiovasc Diabetol

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“…It should be noted that many of these factors have also been linked to muscle atrophy and that obesity-associated muscle atrophy is known to exacerbate sarcopenia (172). For instance, Ang-II, suggested to induce muscle atrophy via NOX2 (4,63), also caused insulin resistance in incubated rat soleus muscles via a mechanism partially alleviated by the antioxidant tempol (84). Thus, a contribution of NOX2mediated oxidative stress might be speculated to be a contributor to both skeletal muscle insulin resistance and atrophy.…”

Section: Redox Signaling In Muscle Insulin Resistancementioning

confidence: 99%

The Emerging Roles of Nicotinamide Adenine Dinucleotide Phosphate Oxidase 2 in Skeletal Muscle Redox Signaling and Metabolism

Henríquez‐Olguín

Boronat

Cabello-Verrugio

et al. 2019

Antioxidants & Redox Signaling

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Significance: Skeletal muscle is a crucial tissue to whole-body locomotion and metabolic health. Reactive oxygen species (ROS) have emerged as intracellular messengers participating in both physiological and pathological adaptations in skeletal muscle. A complex interplay between ROS-producing enzymes and antioxidant networks exists in different subcellular compartments of mature skeletal muscle. Recent evidence suggests that nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (NOXs) are a major source of contraction-and insulin-stimulated oxidants production, but they may paradoxically also contribute to muscle insulin resistance and atrophy. Recent Advances: Pharmacological and molecular biological tools, including redox-sensitive probes and transgenic mouse models, have generated novel insights into compartmentalized redox signaling and suggested that NOX2 contributes to redox control of skeletal muscle metabolism. Critical Issues: Major outstanding questions in skeletal muscle include where NOX2 activation occurs under different conditions in health and disease, how NOX2 activation is regulated, how superoxide/hydrogen peroxide generated by NOX2 reaches the cytosol, what the signaling mediators are downstream of NOX2, and the role of NOX2 for different physiological and pathophysiological processes. Future Directions: Future research should utilize and expand the current redox-signaling toolbox to clarify the NOX2-dependent mechanisms in skeletal muscle and determine whether the proposed functions of NOX2 in cells and animal models are conserved into humans.

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“…Previous work indicates that the TGF-β1-induced rise in ROS production is dependent on NOX in skeletal muscle cells [20]. Other groups demonstrate that Ang-(1-7) decreases mRNA levels of NOX in adipocytes [49] or the NOX activation [57,58].…”

Section: Discussionmentioning

confidence: 96%

“…Studies indicate that the levels of TGF-β1 primarily increase in cases of chronic diseases such as cancer, heart failure, or diabetes [13][14][15][16][17][18], and this increase could cause skeletal muscle atrophy [19]. Our recent research elucidated the mechanism involved in the atrophic effect of TGF-β1 in skeletal muscle, which depends on an increase in reactive oxygen species (ROS) [11,20]. We have shown the over-activation of ubiquitin-proteasome pathway (UPP), specifically an increase in the expression of E3 ubiquitin ligase MuRF-1.…”

Section: Introductionmentioning

confidence: 99%

Angiotensin-(1-7) Prevents Skeletal Muscle Atrophy Induced by Transforming Growth Factor Type Beta (TGF-β) via Mas Receptor Activation

Ábrigo

Simón

Cabrera

et al. 2016

Cell Physiol Biochem

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Background: Transforming growth factor type beta 1 (TGF-β1) produces skeletal muscle atrophy. Angiotensin-(1-7) (Ang-(1-7)), through the Mas receptor, prevents the skeletal muscle atrophy induced by sepsis, immobilization, or angiotensin II (Ang-II). However, the effect of Ang-(1-7) on muscle wasting induced by TGF-β1 is unknown. Aim: To evaluate whether Ang-(1-7)/Mas receptor axis could prevent the skeletal muscle atrophy induced by TGF-β1. Methods: This study assessed the atrophic effect of TGF-β1 in C₂C₁₂ myotubes and mice in absence or presence of Ang-(1-7), and the receptor participation using A779, an antagonist of the Mas receptor. The levels of myosin heavy chain (MHC), polyubiquitination, and MuRF-1 were detected by western blot. Myotube diameter was also evaluated. In vivo analysis included the muscle strength, fibre diameter, MHC and MuRF-1 levels by western blot, and ROS levels by DCF probe detection. Results: The results showed that Ang-(1-7) prevented the increase in MuRF-1 and polyubiquitined protein levels, the decrease of MHC levels, the myotubes/fibre diameter diminution, and the increased production of reactive oxygen species (ROS) induced by TGF-β1. Utilizing A779 inhibited the anti-atrophic effect of Ang-(1-7). Conclusion: The preventive effect of Ang-(1-7) on skeletal muscle atrophy induced by TGF-β1 is produced through inhibition of ROS production and proteasomal degradation of MHC.

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Apocynin inhibits the upregulation of TGF-β1 expression and ROS production induced by TGF-β in skeletal muscle cells

Cited by 14 publications

References 39 publications

Apocynin influence on oxidative stress and cardiac remodeling of spontaneously hypertensive rats with diabetes mellitus

Apocynin influence on oxidative stress and cardiac remodeling of spontaneously hypertensive rats with diabetes mellitus

The Emerging Roles of Nicotinamide Adenine Dinucleotide Phosphate Oxidase 2 in Skeletal Muscle Redox Signaling and Metabolism

Angiotensin-(1-7) Prevents Skeletal Muscle Atrophy Induced by Transforming Growth Factor Type Beta (TGF-β) via Mas Receptor Activation

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