Combined Cornus Officinalis and Paeonia Lactiflora Pall Therapy Alleviates Rheumatoid Arthritis by Regulating Synovial Apoptosis via AMPK-Mediated Mitochondrial Fission

Huang, Lichuang; Hu, Shaoqi; Shao, Meiyu; Wu, Xing-Zheng; Zhang, Jida; Cao, Gang

doi:10.3389/fphar.2021.639009

Cited by 13 publications

(7 citation statements)

References 42 publications

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“…However, different studies have reported different results, with some showing that inhibition of dynamin 1-like protein expression and mitochondrial division can inhibit mitophagy and alleviate inflammatory response in RA ( 301 ). However, some studies have reported contrasting results ( 260 ). This may be related to the diversity of mitochondrial division forms and great variations in the outcomes caused by different division forms ( 302 ).…”

Section: Summary and Discussionmentioning

confidence: 99%

“…The combination of Cornus officinalis and Paeonia lactiflora was effective in ameliorating oxidative stress and inflammation in CIA rats, a process associated with the regulation of AMPK-mediated mitochondrial homeostasis. Apoptosis of synovial cells may be involved in the treatment ( 260 ). Mitochondria are closely related to the cell cycle and play key roles in apoptosis ( 261 , 262 ).…”

Section: Targeting Ros or Mitochondria In Ra Therapy Drugsmentioning

confidence: 99%

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Role of reactive oxygen species and mitochondrial damage in rheumatoid arthritis and targeted drugs

et al. 2023

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Rheumatoid arthritis (RA) is an autoimmune disease characterized by synovial inflammation, pannus formation, and bone and cartilage damage. It has a high disability rate. The hypoxic microenvironment of RA joints can cause reactive oxygen species (ROS) accumulation and mitochondrial damage, which not only affect the metabolic processes of immune cells and pathological changes in fibroblastic synovial cells but also upregulate the expression of several inflammatory pathways, ultimately promoting inflammation. Additionally, ROS and mitochondrial damage are involved in angiogenesis and bone destruction, thereby accelerating RA progression. In this review, we highlighted the effects of ROS accumulation and mitochondrial damage on inflammatory response, angiogenesis, bone and cartilage damage in RA. Additionally, we summarized therapies that target ROS or mitochondria to relieve RA symptoms and discuss the gaps in research and existing controversies, hoping to provide new ideas for research in this area and insights for targeted drug development in RA.

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Section: Summary and Discussionmentioning

confidence: 99%

Section: Targeting Ros or Mitochondria In Ra Therapy Drugsmentioning

confidence: 99%

Role of reactive oxygen species and mitochondrial damage in rheumatoid arthritis and targeted drugs

et al. 2023

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“…Triterpenoid acids derived from Cor could improve hyperlipidemia and hyperglycemia by activating AMPK pathway and its downstream proteins in diabetic mice (Han et al, 2020). Furthermore, according to Huang et al (2021), treatment with a combination of Cor and Paeonia lactiflora Pall alleviates rheumatoid arthritis by AMPK-mediated mitochondrial fission regulating synovial cell apoptosis, suggesting that Cor may improve mitochondrial functions by regulating AMPK pathway. Our animal study has shown that Cor alleviates myocardial mitochondrial abnormalities and processes by activating the APMK pathway, thereby prevention of HF.…”

Section: Discussionmentioning

confidence: 99%

Cornus officinalis Sieb. et Zucc. Alleviates Mitochondrial Abnormalities and Heart Failure through AMPK

Chen,

Chen

et al. 2023

Pharmacognosy Magazine

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Background: Traditional Chinese medicine (TCM) has clear advantages in stabilizing patients with heart failure (HF) and improving cardiac functions. Aims: This study aimed to investigate the role of Cornus officinalis Sieb. et Zucc. (Cor) in HF. Settings and Design: Rats with HF were treated with Cor or Cor with an adenosine monophosphate-activated protein kinase (AMPK) inhibitor, dorsomorphin dihydrochloride (Dor). Materials and Methods: The weight and echocardiography findings of the rats were examined. AMPK and p-AMPK expression levels were assessed using Western blots, mitochondrial changes were evaluated using transmission electron microscopy (TEM), and adenosine triphosphate (ATP) levels were detected in each group. Finally, the targets of Cor were analyzed using HERB ( http://herb.ac.cn ). Statistical Analysis Used: A Student’s t-test was used to compare two groups, and a one-way analysis of variance was performed for intergroup comparison. A p < 0.05 indicated that the difference was statistically significant. Results: Compared with that of the Sham group, the body weight of the Model group decreased; left ventricular end diastolic diameter (LVIDd) and left ventricular end systolic diameter (LVIDs) increased; and left ventricular end diastolic posterior wall thickness (LVPWd), left ventricular end systolic posterior wall thickness (LVPWs), left ventricular ejection fraction (EF), and stroke volume (SV) decreased. These effects were reversed by the Cor treatment. Western blot analysis indicated p-AMPK levels were higher in the Model group than those in the Sham group. After Cor treatment, p-AMPK levels increased but later decreased after treatment with Dor. In addition, myocardial mitochondrial abnormalities were reduced and ATP levels increased in the Cor group compared with the Model group, which were reversed by Dor. Lastly, Cor was found to target AMPK pathway-related genes. Conclusion: Cor exerts protective effects on HF by activating AMPK to improve mitochondrial function.

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“…The pharmacological effects of PF include anti-inflammatory, immune regulation, antioxidant, antitumor and neuroprotective effects (Zhang and Wei, 2020;Wang et al, 2021). Several previous studies have shown that PF improves oxidative stress and mitochondrial dysfunction via activation of AMPK signaling pathways (Zhu et al, 2018;Huang et al, 2021). Nevertheless, the effects and mechanism of PF on CKD skeletal muscle atrophy have not been clearly elucidated.…”

Section: Introductionmentioning

confidence: 99%

Paeoniflorin Ameliorates Skeletal Muscle Atrophy in Chronic Kidney Disease via AMPK/SIRT1/PGC-1α-Mediated Oxidative Stress and Mitochondrial Dysfunction

Huang

et al. 2022

Front. Pharmacol.

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Skeletal muscle atrophy is a common and serious complication of chronic kidney disease (CKD). Oxidative stress and mitochondrial dysfunction are involved in the pathogenesis of muscle atrophy. The aim of this study was to explore the effects and mechanisms of paeoniflorin on CKD skeletal muscle atrophy. We demonstrated that paeoniflorin significantly improved renal function, calcium/phosphorus disorders, nutrition index and skeletal muscle atrophy in the 5/6 nephrectomized model rats. Paeoniflorin ameliorated the expression of proteins associated with muscle atrophy and muscle differentiation, including muscle atrophy F-box (MAFbx/atrogin-1), muscle RING finger 1 (MuRF1), MyoD and myogenin (MyoG). In addition, paeoniflorin modulated redox homeostasis by increasing antioxidant activity and suppressing excessive accumulation of reactive oxygen species (ROS). Paeoniflorin alleviated mitochondrial dysfunction by increasing the activities of electron transport chain complexes and mitochondrial membrane potential. Furthermore, paeoniflorin also regulates mitochondrial dynamics. Importantly, paeoniflorin upregulated the expression of silent information regulator 1 (SIRT1), peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α), and phosphorylation of AMP-activated protein kinase (AMPK). Similar results were observed in C2C12 myoblasts treated with TNF-α and paeoniflorin. Notably, these beneficial effects of paeoniflorin on muscle atrophy were abolished by inhibiting AMPK and SIRT1 and knocking down PGC-1α. Taken together, this study showed for the first time that paeoniflorin has great therapeutic potential for CKD skeletal muscle atrophy through AMPK/SIRT1/PGC-1α-mediated oxidative stress and mitochondrial dysfunction.

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Combined Cornus Officinalis and Paeonia Lactiflora Pall Therapy Alleviates Rheumatoid Arthritis by Regulating Synovial Apoptosis via AMPK-Mediated Mitochondrial Fission

Cited by 13 publications

References 42 publications

Role of reactive oxygen species and mitochondrial damage in rheumatoid arthritis and targeted drugs

Role of reactive oxygen species and mitochondrial damage in rheumatoid arthritis and targeted drugs

Cornus officinalis Sieb. et Zucc. Alleviates Mitochondrial Abnormalities and Heart Failure through AMPK

Paeoniflorin Ameliorates Skeletal Muscle Atrophy in Chronic Kidney Disease via AMPK/SIRT1/PGC-1α-Mediated Oxidative Stress and Mitochondrial Dysfunction

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