Berberine Alleviates the Damage, Oxidative Stress and Mitochondrial Dysfunction of PC12 Cells Induced by High Glucose by Activating the KEAP1/Nrf2/ARE Pathway

Yuan, Haoyu; Wang, Baohua; Zicheng, Ye; Li, Saimei

doi:10.1007/s12033-022-00651-5

Cited by 6 publications

(2 citation statements)

References 39 publications

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“…Studies have suggested that berberine regulates the activity of the mitochondrial respiratory chain, which is responsible for generating ATP and stimulating mitochondrial biogenesis [ 30 , 31 ]. Berberine also possesses antioxidant properties, which can help protect mitochondria from oxidative stress [ 15 , 32 ]. In the present study, we showed that berberine improved mitochondrial function through the stimulation of mitophagy.…”

Section: Discussionmentioning

confidence: 99%

“…mt-Keima fluorescence was imaged using two sequential excitation lasers (458 nm and 561 nm) and a 595–700 nm emission bandwidth. Quantitation of mitophagy levels based on mt-Keima confocal images was performed using Zeiss Zen software (Zen 3.0 SR) as described previously [ 32 , 49 ]. We depicted the mt-Keima fluorescence signal from the 458 nm excitation wavelength in green and the signal from excitation by the 561 nm laser in red.…”

Section: Methodsmentioning

confidence: 99%

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Berberine Induces Mitophagy through Adenosine Monophosphate-Activated Protein Kinase and Ameliorates Mitochondrial Dysfunction in PINK1 Knockout Mouse Embryonic Fibroblasts

Um,

Lee,

Kim

et al. 2023

IJMS

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Mitophagy stimulation has been shown to have a therapeutic effect on various neurodegenerative diseases. However, nontoxic mitophagy inducers are still very limited. In this study, we found that the natural alkaloid berberine exhibited mitophagy stimulation activity in various human cells. Berberine did not interfere with mitochondrial function, unlike the well-known mitophagy inducer carbonyl cyanide m-chlorophenyl hydrazone (CCCP), and subsequently induced mitochondrial biogenesis. Berberine treatment induced the activation of adenosine monophosphate-activated protein kinase (AMPK), and the AMPK inhibitor compound C abolished berberine-induced mitophagy, suggesting that AMPK activation is essential for berberine-induced mitophagy. Notably, berberine treatment reversed mitochondrial dysfunction in PINK1 knockout mouse embryonic fibroblasts. Our results suggest that berberine is a mitophagy-specific inducer and can be used as a therapeutic treatment for neurodegenerative diseases, including Parkinson’s disease, and that natural alkaloids are potential sources of mitophagy inducers.

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