Effects of high intensity exhaustive exercise on SOD, MDA, and NO levels in rats with knee osteoarthritis

Li, X.D.; Sun, Gwo‐Ching; Zhu, Wentao; Wang, Y.H.

doi:10.4238/2015.october.16.3

Cited by 33 publications

(24 citation statements)

References 19 publications

(17 reference statements)

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“…Lipid peroxidation and bodily damage are also concomitantly increased. Under normal conditions, SOD1 release would also gradually increase to maintain the balance between oxidation and antioxidation (30). Before the experiment, we predicted that under the oxidative stress of the model group, the activity and the transcription, as well as the translation of SOD1 would be lower than that of the untreated group, and that of one or more UA-treated groups would be higher than the model group; however, in this study, we did not observe this phenomenon.…”

Section: Discussionmentioning

confidence: 99%

Influence of different concentrations of uric acid on oxidative stress in steatosis hepatocytes

Cheng

Yang²,

Zhou

et al. 2018

Exp Ther Med

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Abstract. The development of nonalcoholic fatty liver disease (NAFLD) is caused by the steatosis of hepatocytes, which induces oxidative stress (OS). Thus, OS has an important role in the development of NAFLD. In the present study, the L-02 hepatocyte cell line was used to develop a steatosis cell model. The best model was determined using an MTT assay and the triglyceride levels. Model cells were treated with high concentrations of uric acid (UA; 0, 5, 10, 20 and 30 mg/dl) for 24, 48, 72 and 96 h. Indicators of oxidation were then measured, which included total superoxide dismutase (SOD), malonaldehyde (MDA) and reduced glutathione (GSH), and the transcriptional and translational levels of SOD1 and γ-glutamate-cysteine ligase (γ-GCLC) were also determined. In addition, the intracellular levels of aspartate aminotransferase and alanine aminotransferase (ALT) were detected. The activity of SOD1 decreased over time and the result was supported by the results of western blotting. The transcriptional levels of SOD1 in model cells was significantly higher than untreated cells at 48 h. With the decreased levels of SOD1 and GSH, MDA increased in a time-dependent manner. The content of GSH decreased with time as well, which was also reflected in the results of western blotting. The transcriptional levels of γ-GCLC in all UA-treated groups were lower when compared with those observed in the model group. The activity of ALT tended to increase, depending on the duration of treatment. Treatment with 5 and 10 mg/dl UA had an antioxidative effect on the model cells, and 30 mg/dl UA treatment for 48 h increased OS in the cells.

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Section: Discussionmentioning

confidence: 99%

Influence of different concentrations of uric acid on oxidative stress in steatosis hepatocytes

Cheng

Yang²,

Zhou

et al. 2018

Exp Ther Med

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“…Inflammation of joints and oxidative stress promote each other: the inflammation of joints produces a large amount of reactive oxygen free radicals, and a large amount of oxygen free radicals in turn contribute to the pathological occurrence and development of long-lasting inflammation (Sabina, Rasool, Mathew, Ezilrani, & Indu, 2010). Notably, superoxide dismutase (SOD) active molecule is a major free radical scavenger that can significantly reduce free radical damage to articular cartilage (X. D. Li, Sun, Zhu, & Wang, 2015).…”

Section: Introductionmentioning

confidence: 99%

Protective effects of quercetin against inflammation and oxidative stress in a rabbit model of knee osteoarthritis

Wei

Zhang

Tang

et al. 2019

Drug Development Research

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Hit, Lead & Candidate Discovery This study investigated the effects of a natural phenolic compound quercetin on surgical‐induced osteoarthritis (OA) in rabbits. Forty‐eight New Zealand White rabbits were used to establish OA model by Hulth modified method, and subsequently randomized into untreated OA group (treatment was drinking water), celecoxib treated group (celecoxib 100 mg kg‑1 by gavage), and quercetin treated group (25 mg kg‑1 by gavage). Sixteen nonoperated rabbits served as the normal controls (drinking water was given). The treatment (length: 4 weeks) started on the 5th week postoperation when the OA pathological changes were manifested. Expressions of superoxide dismutase (SOD), matrix metalloproteinase‐13 (MMP‐13) and tissue inhibitor of metalloproteinases‐1 (TIMP‐1) in serum, synovial fluid, and synovial tissue were measured at 8 and 12 weeks postoperation. Pathological analysis was performed with synovial tissue section and Osteoarthritis Research Society International histopathology grading and staging scores were determined. The quercetin treated group showed higher SOD and TIMP‐1 expressions but lower MMP‐13 expression than untreated OA group in the serum, synovial fluid and synovial tissues (p < .05). There was no significant difference in the SOD, MMP‐13 and TIMP‐1 expressions between the quercetin‐treated and celecoxib‐treated groups. The MMP‐13/TIMP‐1 ratio of the quercetin treated group was significantly lower than that of the untreated OA group (p < .05). Quercetin can up‐regulate SOD and TIMP‐1, down‐regulate MMP‐13, and improve the degeneration of OA through weakening the oxidative stress responses and inhibiting the degradation of cartilage extracellular matrix.

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“…It should be highlighted though, that exercise induces intensity-, duration-and type-dependent effects on antioxidant mechanisms and oxidative stress levels. Very intense or exhaustive exercise (either acute or prolonged) increases oxidation and downregulates the antioxidant defense resulting in excessive damage to macromolecules [61,62], whereas low-to-moderate intensity exercise (particularly repeated exercise bouts) enhances the activity of antioxidant enzymes and consequently lowers the levels of generated ROS and improves the cellular adaptation to subsequent stress [63,64]. For instance, a significant decrease in SOD, GPx, and catalase activity has been reported following exhaustive high intensity exercise [61,62], while an 8-week training program of moderate intensity resulted in improved total antioxidant capacity and reduce lipid oxidation [65].…”

Section: Antioxidants Oxidative Stress and Cardiovascular Diseasementioning

confidence: 99%

“…Sepifically, Li et al [61] found that following 12 weeks of progressive RE training, phosphorylation of AKT and eNOS as well as expression of redox factor 1 and MnSOD were significantly elevated while FOXO1 phosphorylation decreased in rat aorta, providing evidence that RE can improve the function of the aorta and preserve redox status. By utilizing a rat model, Camiletti-Moiron et al [232,233] also noted an antioxidant effect of RE, reporting increased catalase activity following a 12-week intervention with high-intensity RE training, despite no alteration was observed for the other antioxidant enzymes measured, such as MnSOD and Cu/ZnSOD.…”

Section: Regular Resistance Exercise Trainingmentioning

confidence: 99%

Exercise-Induced Regulation of Redox Status in Cardiovascular Diseases: The Role of Exercise Training and Detraining

et al. 2019

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Although low levels of reactive oxygen species (ROS) are beneficial for the organism ensuring normal cell and vascular function, the overproduction of ROS and increased oxidative stress levels play a significant role in the onset and progression of cardiovascular diseases (CVDs). This paper aims at providing a thorough review of the available literature investigating the effects of acute and chronic exercise training and detraining on redox regulation, in the context of CVDs. An acute bout of either cardiovascular or resistance exercise training induces a transient oxidative stress and inflammatory response accompanied by reduced antioxidant capacity and enhanced oxidative damage. There is evidence showing that these responses to exercise are proportional to exercise intensity and inversely related to an individual's physical conditioning status. However, when chronically performed, both types of exercise amplify the antioxidant defense mechanism, reduce oxidative stress and preserve redox status. On the other hand, detraining results in maladaptations within a time-frame that depends on the exercise training intensity and mode, as high-intensity training is superior to low-intensity and resistance training is superior to cardiovascular training in preserving exercise-induced adaptations during detraining periods. Collectively, these findings suggest that exercise training, either cardiovascular or resistance or even a combination of them, is a promising, safe and efficient tool in the prevention and treatment of CVDs.

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Effects of high intensity exhaustive exercise on SOD, MDA, and NO levels in rats with knee osteoarthritis

Cited by 33 publications

References 19 publications

Influence of different concentrations of uric acid on oxidative stress in steatosis hepatocytes

Influence of different concentrations of uric acid on oxidative stress in steatosis hepatocytes

Protective effects of quercetin against inflammation and oxidative stress in a rabbit model of knee osteoarthritis

Exercise-Induced Regulation of Redox Status in Cardiovascular Diseases: The Role of Exercise Training and Detraining

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