Propofol protects human cardiac cells against chemical hypoxiainduced injury by regulating the JNK signaling pathways

Abstract

Propofol is a widely used intravenous anesthetic shown to exert a cardioprotective role against oxidative stress and ischemia/reperfusion injury in rat cardiac H9c2 cells. However, the regulatory mechanisms and functions of propofol in human cardiomyocytes remain unknown. The present study chemically induced hypoxia with cobalt chloride (CoCl 2 ) to mimic cardiomyocyte ischemic injury in human cardiac AC16 and HCM cells. To investigate its underlying mechanisms, propofol was added to the cells before the chemical hypoxia phase. The present results suggested that, in response to hypoxia, mitochondrial membrane potential was lost, and cardiomyocyte viability and superoxide dismutase levels decreased. However, the present results showed that reactive oxygen species and malondialdehyde levels increased. The present results suggested that these effects were significantly reversed following propofol treatment. Additionally, the present results suggested that the protective effect of propofol against CoCl 2 -induced injury may be inhibited by the activation of the JNK signaling pathways. The present results indicated that propofol pre-treatment inhibited CoCl 2 -induced myocardial injury by preventing mitochondrial dysfunction, which may be partially due to the activation of the JNK signaling pathways. Therefore, propofol may exert anti-oxidative effects in human cardiac cells. The present results suggested that propofol may be used as a treatment for oxidative stress-related cardiac disorders.

Propofol via Antioxidant Property Attenuated Hypoxia-Mediated Mitochondrial Dynamic Imbalance and Malfunction in Primary Rat Hippocampal Neurons

“…In the current study, we focused on the effect and mechanism of propofol on mitochondrial malfunction and dynamic imbalance, which were induced by hypoxia in hippocampal neurons. In consistence with previous publications carried out in cardiac cells [ 52 ], hepatic cells [ 53 ], and microglia [ 54 ], we proved propofol may protect hypoxia-induced mitochondrial malfunction and dynamic imbalance through its antioxidant property in hippocampal neurons ( Figure 3 ).…”

Signaling pathways in the treatment of Alzheimer’s disease with acupuncture: a narrative review

“…46 Studies have shown that stimulating JNK and p38-MAPK has a proapoptotic effect, whereas activating ERK has an anti-apoptotic effect following the activation of the MAPK signaling cascade, which is closely associated with cellular apoptosis, autophagy, inflammation and oxidative stress. [47][48][49] The MAPK signaling pathway may play a significant role in the occurrence and development of AD. A positive association has been found between the disease and increased levels of p-p38MAPK and p-JNK in the blood of AD patients.…”

Anesthesia‐Induced Oxidative Stress: Are There Differences between Intravenous and Inhaled Anesthetics?

“…In summary, this study demonstrated that propofol influences both levels of oxidative stress and inflammation [ 62 ]. The antioxidative properties of propofol were also observed in human cardiac cells, and the protective effect was attributed to an activation of the JNK signaling pathway [ 64 ].…”