Capillarisin attenuates exercise-induced muscle damage through MAPK and NF-κB signaling

Kim, Minjee; Chun, Jaemoo; Jung, Hyun Ah; Choi, Jae Sue; Kim, Yeong Shik

doi:10.1016/j.phymed.2017.04.007

Cited by 17 publications

(6 citation statements)

References 21 publications

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“…We have also looked at the post-exercise changes of muscle damage markers and we found a small non-significant numerical increase in these markers during the recovery from exercise. Even small changes in creatine kinase activity during exercise seem to confirm the effect of exercise on the integrity of muscle cells, which is consistent with earlier studies performed by other authors but in different populations and different experimental conditions [30,31].…”

Section: Discussionsupporting

confidence: 91%

Effect of short-term physical exercise on serum markers of skeletal muscle damage in hypertensive patients treated with a combination of statin and angiotensin-converting enzyme inhibitor

Deska¹,

Nowicki

2019

Arterial Hypertension

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Background. Muscle strain during physical exercise may lead to muscle damage and hyperkalaemia. Commonly prescribed drugs including statins and angiotensin-converting enzyme inhibitors (ACEI) may increase serum potassium and cause muscle damage. We postulated that the risk may be even higher if the patients are treated with a combination of statin and ACEI. The aim of the study was to compare the effect of moderate intensity short-term physical exercise on the changes of muscle injury markers serum carbonic anhydrase 3 and creatine kinase in patients with arterial hypertension receiving ACEI and statin. Material and methods. Eighteen patients with arterial hypertension treated with ACEI were included in a prospective placebo-controlled cross-over study. 18 healthy individuals served as controls. Hypertensive patients underwent 30-minute exercise test, which was repeated two times in a random order after the administration of ACEI with statin or ACEI with placebo. Each treatment period lasted 8 weeks separated by 2-week wash-out. Normotensive subjects underwent a single exercise test. Serum carbonic anhydrase 3 (CAIII) and creatine kinase (CK) activity were measured before and after exercise and recovery. Results. At baseline and during the exercise CAIII was significantly higher in healthy volunteers compared to hypertensive patients. CAIII increased significantly during exercise only after treatment with both ACEI and statin. Serum CK was higher in hypertensive patients treated with ACEI plus statin during all exercise tests. Conclusions. Addition of statin to ACEI in patients with arterial hypertension does not increase the risk of muscle damage during moderate intensity short-term physical exercise.

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Section: Discussionsupporting

confidence: 91%

Effect of short-term physical exercise on serum markers of skeletal muscle damage in hypertensive patients treated with a combination of statin and angiotensin-converting enzyme inhibitor

Deska¹,

Nowicki

2019

Arterial Hypertension

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“…The downstream inflammatory signaling pathway is activated by excessive ROS via the regulation of phosphorylation of extracellular signal-regulated kinase, phosphatidylinositol 3-hydroxy kinase and p38 mitogen-activated protein kinase to impact the expression of terminal gene transcription, protein translation, cell proliferation and apoptosis, and endothelium-dependent vasodilation. [38–40] In addition, oxidative stress directly interacts with nuclear transcription factors to promote the expression of inflammatory proteins. [41]…”

Section: Discussionmentioning

confidence: 99%

Relationship between oxidative stress and inflammation in hyperuricemia

Zhou

Zhao²,

Pu³

et al. 2018

Medicine

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The average age of hyperuricemia patients has gradually decreased, but young patients with primary hyperuricemia often do not exhibit clinical symptoms and have not received sufficient attention. However, a lack of symptoms with primary hyperuricemia does not mean that high serum uric acid (UA) levels cannot lead to pathological effects, such as oxidative stress and inflammation, and the specific damage is still unclear. We aimed to determine the relationship between oxidative stress and inflammation to explore the possible role of pathological damage in asymptomatic young patients with primary hyperuricemia.A total of 333 participants were enrolled in our study: 158 asymptomatic young patients with primary hyperuricemia and 175 healthy persons from a health check-up population. Malondialdehyde (MDA), superoxide dismutase (SOD), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and general biochemical markers were measured.We found no differences in biochemical markers (fasting glucose, TG, TC, LDL-C, HDL-C, SCr, BUN, AST, and ALT) between the patients and healthy persons. Subsequent analyses of oxidative stress and inflammation revealed that the serum levels of MDA, IL-6, and TNF-α in the patients were significantly higher than those in the healthy control group (P < .001), and the SOD activity was significantly lower (P < .001). As the UA levels increased, MDA increased significantly and SOD decreased significantly; likewise, IL-6 and TNF-α increased significantly as the UA level increased. MDA showed a significant positive correlation with IL-6 (r = 0.367, P < .001) and TNF-α (r = 0.319, P < .001), and SOD was negatively correlated with IL-6 (r = −0.241, P < .01) and TNF-α (r = −0.308, P < .001). Multivariable logistic regression analysis showed that UA (OR: 2.379, 95% CI: 1.698–3.286, P < .001; OR: 3.261, 95% CI: 1.729–3.857, P < .001; for IL-6 and TNF-α, respectively) and MDA (OR: 1.836, 95% CI: 1.283–2.517, P < .01; OR: 2.532, 95% CI: 1.693–3.102, P < .001; for IL-6 and TNF-α, respectively) were risk factors for high IL-6 and TNF-α and that SOD (OR: 0.517, 95% CI: 0.428–0.763, P < .01; OR: 0.603, 95% CI: 0.415–0.699, P < .001; for IL-6 and TNF-α, respectively) was a protective factor.In our study, some abnormal pathological effects were found in asymptomatic young patients with hyperuricemia, suggesting that in young hyperuricemia patients, oxidative stress, inflammation and the inflammatory response may be related to the oxidative stress induced by UA. Therefore, we should pay more attention to the pathological damage caused by these alterations.

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“…Since heat processing is used to promote drug effectiveness and safety in herbal medicine, we provide evidence that HPAC decreases inflammatory responses. Previous studies have shown that pure capillarisin (CAP) isolated from AC showed muscle protective effect through MAPK and NF- κ B signaling [ 79 ]. HPAC exhibits similar effects but its anti-inflammatory effect is through regulating I κ B α phosphorylation and NF- κ B activation via HO-1 induction.…”

Section: Discussionmentioning

confidence: 99%

Anti-Inflammatory Effects of Heat-Processed Artemisia capillaris Thunberg by Regulating IκBα/NF-κB Complex and 15-PGDH in Mouse Macrophage Cells

Ali¹,

Lim

Kim

et al. 2021

Evidence-Based Complementary and Alternative Medicine

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Growing evidence suggests that dietary nutrients in herbs and plants are beneficial in improving inflammatory disorders. Artemisia capillaris Thunberg (AC) is a traditional herbal medicine widely used in East Asia to treat pain, hepatotoxicity, and inflammatory disorders. Heat processing is a unique pharmaceutical method used in traditional herbal medicine to enhance the pharmacological effects and safety of medicinal plants. This study demonstrates the anti-inflammatory effects of heat-processed AC (HPAC) in lipopolysaccharide- (LPS-) treated mouse macrophage cells. HPAC reduced LPS-induced inflammatory mediators such as IL-6, IL-1β, TNF-α, NO, and PGE2 in RAW 264.7 cells. Interestingly, 15-PGDH appears to play a pivotal role rather than COX-2 and mPGES-1 when HPAC regulated PGE2 levels. Meanwhile, HPAC showed anti-inflammatory effects by blocking IκBα phosphorylation and NF-κB nuclear translocalization. Also, we found that HO-1 upregulation was mediated by the mitogen-activated protein kinase (MAPK) pathways in HPAC-treated RAW 264.7 cells. And, in RAW 264.7 cells challenged with LPS, HPAC restored HO-1 expression, leading to NF-κB inhibition. Through further experiments using specific MAPK inhibitors, we found that, in response to LPS, the phosphorylated IκBα and activated NF-κB were attenuated by p38 MAPK/HO-1 pathway. Therefore, HPAC targeting both the IκBα/NF-κB complex and 15-PGDH may be considered as a potential novel anti-inflammatory agent derived from a natural source.

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Capillarisin attenuates exercise-induced muscle damage through MAPK and NF-κB signaling

Cited by 17 publications

References 21 publications

Effect of short-term physical exercise on serum markers of skeletal muscle damage in hypertensive patients treated with a combination of statin and angiotensin-converting enzyme inhibitor

Effect of short-term physical exercise on serum markers of skeletal muscle damage in hypertensive patients treated with a combination of statin and angiotensin-converting enzyme inhibitor

Relationship between oxidative stress and inflammation in hyperuricemia

Anti-Inflammatory Effects of Heat-Processed Artemisia capillaris Thunberg by Regulating IκBα/NF-κB Complex and 15-PGDH in Mouse Macrophage Cells

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