Inhibition of Drp1-dependent mitochondrial fission by natural compounds as a therapeutic strategy for organ injuries

Rahmani, Sohrab; Roohbakhsh, Ali; Karimi, Gholamreza

doi:10.1016/j.phrs.2023.106672

Cited by 12 publications

(3 citation statements)

References 91 publications

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“… 33 DRP1 dynamically regulates mitochondrial morphology, with its recruitment to the outer mitochondrial membrane being critical for mitochondrial fission. 34 We observed that QDN enhanced mitochondrial fission, evidenced by increased mitochondrial fragments and enhanced levels of mitochondrial fission protein DRP1. Mdivi‐1, an inhibitor of mitochondrial division, effectively blocked QDN‐mediated mitochondrial division and apoptosis by treatment of NSCLC cells.…”

Section: Discussionmentioning

confidence: 74%

“…Mitochondrial fragmentation from fission is tightly linked to apoptosis, and a balance shift in mitochondrial morphology to fission increases susceptibility to cell death 33 . DRP1 dynamically regulates mitochondrial morphology, with its recruitment to the outer mitochondrial membrane being critical for mitochondrial fission 34 . We observed that QDN enhanced mitochondrial fission, evidenced by increased mitochondrial fragments and enhanced levels of mitochondrial fission protein DRP1.…”

Section: Discussionmentioning

confidence: 75%

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QiDongNing induces lung cancer cell apoptosis via triggering P53/DRP1‐mediated mitochondrial fission

Ding,

Wang,

et al. 2024

J Cellular Molecular Medi

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Non‐small‐cell lung cancer (NSCLC) is a major cause of worldwide cancer death, posing a challenge for effective treatment. Our previous findings showed that Chinese herbal medicine (CHM) QiDongNing (QDN) could upregulate the expression of p53 and trigger cell apoptosis in NSCLC. Here, our objective was to investigate the mechanisms of QDN‐induced apoptosis enhancement. We chose A549 and NCI‐H460 cells for validation in vitro, and LLC cells were applied to form a subcutaneous transplantation tumour model for validation in more depth. Our findings indicated that QDN inhibited multiple biological behaviours, including cell proliferation, cloning, migration, invasion and induction of apoptosis. We further discovered that QDN increased the pro‐apoptotic BAX while inhibiting the anti‐apoptotic Bcl2. QDN therapy led to a decline in adenosine triphosphate (ATP) and a rise in reactive oxygen species (ROS). Furthermore, QDN elevated the levels of the tumour suppressor p53 and the mitochondrial division factor DRP1 and FIS1, and decreased the mitochondrial fusion molecules MFN1, MFN2, and OPA1. The results were further verified by rescue experiments, the p53 inhibitor Pifithrin‐α and the mitochondrial division inhibitor Mdivi1 partially inhibited QDN‐induced apoptosis and mitochondrial dysfunction, whereas overexpression of p53 rather increased the efficacy of the therapy. Additionally, QDN inhibited tumour growth with acceptable safety in vivo. In conclusion, QDN induced apoptosis via triggering p53/DRP1‐mediated mitochondrial fission in NSCLC cells.

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Section: Discussionmentioning

confidence: 74%

Section: Discussionmentioning

confidence: 75%

QiDongNing induces lung cancer cell apoptosis via triggering P53/DRP1‐mediated mitochondrial fission

Ding,

Wang,

et al. 2024

J Cellular Molecular Medi

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“…To study the effects of glyphosate (GYP, 0.5 mg/L for 30 minutes/ day) for 14 days on zebrafish [20]; donepezil (DP, 1 mg/L for 14 days) exposure to zebrafish [21]; and rutin (50, 100 and 150 µg/L for 30 minutes/day) for 14 days to zebrafish [22].…”

Section: Drug Treatment Schedulementioning

confidence: 99%

"Ameliorative Potential of Rutin on Glyphosate-induced Cognitive Dysfunction in Adult Zebrafish Model via Antioxidant and Acetylcholinesterase Inhibitory Actions"

Muthuraman

2023

BJSTR

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Rutin is a bioflavonoid and plant pigment. It is found in various fruits and vegetables. Chemically, it is known as rutoside, quercetin-3-O-rutinoside, sophorin, and vitamin P. It has antioxidant, anti-inflammatory, and immunomodulation-associated neuroprotective and anti-Alzheimer actions. The role of rutin against glyphosate-induced cognitive dysfunction in adult zebrafish has not been studied yet. The present study focused on the role of rutin on glyphosate-induced cognitive dysfunction in adult zebrafish. The glyphosate (GYP, 0.5 mg/L), rutin (50, 100, and 150 µg/L), and donepezil (DP, 1 µg/mL) for 30 minutes/day were exposed for 14 consecutive days. On the 14th day, the neurobehavioural changes were assessed by three horizontal compartment test, optokinetic motor response (OMR), startle response (SR), and T-maze tests. On the 15th day, animals were sacrificed and brain biomarker changes i.e., brain acetylcholinesterase (AChE) activity, thiobarbituric acid reactive substances (TBARS), and reduced glutathione (GSH) levels were estimated. The exposure to rutin ameliorated the GYP-induced cognitive dysfunctions and changes in tissue biomarkers. The results are similar to DP-exposed animals. Hence, rutin can be useful for the treatment of herbicide toxicity like GYP-associated neurocognitive disorders viz anti-oxidant, anti-lipid peroxidation, and modulatory action of cholinergic neurotransmitter activities.

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The Cardiovascular Protective Function of Natural Compounds Through AMPK/SIRT1/PGC‐1α Signaling Pathway

Rahmani,

Roohbakhsh,

Pourbarkhordar

et al. 2024

Food Science & Nutrition

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Cardiovascular disease (CVD) poses a major risk to human health and exert a heavy burden on individuals, society, and healthcare systems. Therefore, it is critical to identify CVD's underlying mechanism(s) and target them using effective agents. Natural compounds have shown promise as antioxidants with cardioprotective functions against CVD injuries due to their antioxidative solid capacity and high safety profile. Several CVDs, such as heart failure, ischemia/reperfusion, atherosclerosis, and cardiomyopathies, are closely linked to mitochondrial dysfunction. It is well established that activating the AMPK/SIRT1/PGC‐1α pathway during CVD promotes mitochondrial function. Therefore, targeting the AMPK/SIRT1/PGC‐1α pathway provides a foundation for novel therapeutic strategies to combat CVD. A key goal of our search was to find natural compounds that target this biological pathway and have beneficial effects on CVD.

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Inhibition of Drp1-dependent mitochondrial fission by natural compounds as a therapeutic strategy for organ injuries

Cited by 12 publications

References 91 publications

QiDongNing induces lung cancer cell apoptosis via triggering P53/DRP1‐mediated mitochondrial fission

QiDongNing induces lung cancer cell apoptosis via triggering P53/DRP1‐mediated mitochondrial fission

"Ameliorative Potential of Rutin on Glyphosate-induced Cognitive Dysfunction in Adult Zebrafish Model via Antioxidant and Acetylcholinesterase Inhibitory Actions"

The Cardiovascular Protective Function of Natural Compounds Through AMPK/SIRT1/PGC‐1α Signaling Pathway

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