2016
DOI: 10.1016/j.carbpol.2016.06.053
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Chitosan attenuates dibutyltin-induced apoptosis in PC12 cells through inhibition of the mitochondria-dependent pathway

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Cited by 21 publications
(12 citation statements)
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“…Thus, tackling mitochondrial dysfunction offers a promising therapeutic target in neurodegenerative disease. Wang et al discovered that chitosan (CS) could significantly increase the cell viability and decrease the lactate dehydrogenase (LDH) release induced by Dibutyltin (DBT) in a dose-dependent manner [63]. CS could inhibit cell apoptosis, mitochondrial membrane potential (MMP) disruption, and ROS generation in PC12 cells [63].…”
Section: The Potential Protective Effects Of Chitosan and Its Derimentioning
confidence: 99%
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“…Thus, tackling mitochondrial dysfunction offers a promising therapeutic target in neurodegenerative disease. Wang et al discovered that chitosan (CS) could significantly increase the cell viability and decrease the lactate dehydrogenase (LDH) release induced by Dibutyltin (DBT) in a dose-dependent manner [63]. CS could inhibit cell apoptosis, mitochondrial membrane potential (MMP) disruption, and ROS generation in PC12 cells [63].…”
Section: The Potential Protective Effects Of Chitosan and Its Derimentioning
confidence: 99%
“…Wang et al discovered that chitosan (CS) could significantly increase the cell viability and decrease the lactate dehydrogenase (LDH) release induced by Dibutyltin (DBT) in a dose-dependent manner [63]. CS could inhibit cell apoptosis, mitochondrial membrane potential (MMP) disruption, and ROS generation in PC12 cells [63]. Therefore, CS may inhibit DBT-induced apoptosis in PC12 cells through interfering with the mitochondria-dependent pathway [63].…”
Section: The Potential Protective Effects Of Chitosan and Its Derimentioning
confidence: 99%
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