Propofol Suppressed Hypoxia/Reoxygenation‐Induced Apoptosis in HBVSMC by Regulation of the Expression of Bcl‐2, Bax, Caspase3, Kir6.1, and p‐JNK

Zhang, Jianhai; Xia, Yunfei; Xu, Zifeng; Deng, Xiaoming

doi:10.1155/2016/1518738

Cited by 34 publications

(26 citation statements)

References 50 publications

(49 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Apoptosis-Related Genes. Bcl-2 [38], BAX [39], and caspase-3 [40,41] have been reported to be associated with oxidative stress and apoptosis. Infrasound treatment reduced relative mRNA level of Bcl-2 and a sharp increase in relative mRNA levels of bax and caspase-3.…”

Section: The Effects Of Thsg On Relative Mrna Levels Ofmentioning

confidence: 99%

Tetrahydroxystilbene Glucoside Ameliorates Infrasound-Induced Central Nervous System (CNS) Injury by Improving Antioxidant and Anti-Inflammatory Capacity

Zhou

Yang

Fan

et al. 2020

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

Background. Infrasound is a major threat to global health by causing injuries of the central nervous system (CNS). However, there remains no effective therapeutic agent for preventing infrasound-caused CNS injury. 2,3,5,4′-Tetrahydroxystilbene-2-O-β-D-glycoside (THSG) exerts protective function against CNS injuries and may have beneficial effects on infrasound-induced CNS impairment. Methods. A mouse model with CNS (oxidative stress-induced inflammation and neuronal apoptosis) injuries was established when the mouse was exposed to the infrasound of 16 Hz at 130 dB for 2 h each day and the duration of treatment was 8 d. The mice were divided into the control (CG, healthy mice), the model (MG, model mice), and the THSG (EG, experimental group, model mice treated with THSG) groups. The learning and memory impairments caused by infrasound were examined using a Morris water maze test. Lipid profiles, antioxidant biomarkers, and inflammatory cytokines in hippocampus tissue were measured by using corresponding ELISA kits. Meanwhile, BCL-2/BAX/caspase-3 signaling pathway was measured in the hippocampi and prefrontal cortex of the mouse brain using real-time qPCR and Western blot. Nissl’s stain was used to measure neuronal necrosis in the hippocampi and prefrontal cortex of the mouse brain. Results. THSG significantly ameliorated the learning and memory impairments caused by infrasound. On the other hand, THSG improved lipid profiles, increased antioxidant properties by affecting the levels of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT), and malondialdehyde (MDA), and displayed anti-inflammatory action via the downregulation of IL- (interleukin-) 6, IL-8, IL-10, TNF- (tumor necrosis factor-) α, and hs-CRP (high-sensitivity C-reactive protein) in the hippocampal tissues of the mouse model (P<0.05). Additionally, Nissl’s stain showed that THSG inhibited infrasound-induced neuronal necrosis in the hippocampi and prefrontal cortex. Besides, THSG exerted antiapoptosis function by upregulating the level of Bcl-2 and downregulating the levels of BAX and caspase-3 in the hippocampi. Conclusion. THSG may be an effective anti-infrasound drug against CNS injury by improving antioxidant, anti-inflammatory, antiapoptosis, and antinecrosis capacities. Further research is still needed to confirm the exact molecular mechanism.

show abstract

Section: The Effects Of Thsg On Relative Mrna Levels Ofmentioning

confidence: 99%

Tetrahydroxystilbene Glucoside Ameliorates Infrasound-Induced Central Nervous System (CNS) Injury by Improving Antioxidant and Anti-Inflammatory Capacity

Zhou

Yang

Fan

et al. 2020

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

show abstract

“…Furthermore, propofol has an anti-oxidative effect in rat cardiomyocytes and macrophages, which is associated with the suppression of oxidative stress-related enzymes including inducible nitric oxide synthase, superoxide dismutase (SOD) and neutrophil cytosolic factor 1. In addition, propofol is associated with an increase in intracellular nitric oxide release (15,16) and the preservation of Bcl2 expression levels (17). Propofol was shown to protect microglia from hypoxia-induced inflammation and apoptosis by maintaining intracellular Ca 2+ homeostasis and the activation of the JNK1/Stat3 signaling pathway (18).…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2020

View full text Add to dashboard Cite

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.

show abstract

“…Hepatic I/R injury is supposed to be induced by the return of blood flow and restoration of oxygen delivery in ischemic tissues, which aggravates the metabolic dysfunction of tissues instead of restoring their functions. Propofol (2,6-dissopropyl phenol) is a rapid and short-acting general anesthetic and widely used in clinical anesthesia (Zhang et al, 2016). Among them, the formation of ROS and oxidant stress are the main pathological basis of hepatic I/R.…”

Section: Introductionmentioning

confidence: 99%

“…Although the precise mechanisms of hepatic I/R injury have not been illuminated clearly, researchers have developed numerous medicines and methods to attenuate hepatic I/R injury, including anesthetics. Propofol (2,6-dissopropyl phenol) is a rapid and short-acting general anesthetic and widely used in clinical anesthesia (Zhang et al, 2016). Recently, propofol has been found to have a protective effect in I/R injury in the heart, kidney, and liver with the antioxidant effects (Ye et al, 2012;Yingjie et al, 2015;Shirakawa et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

Propofol protects against hepatic ischemia/reperfusion injury via miR‐133a‐5p regulating the expression of MAPK6

Zhao

Meng

et al. 2017

Cell Biology International

View full text Add to dashboard Cite

Propofol has been found to play an important role in hepatic ischemia/reperfusion (I/R) injury with the antioxidant effects. However, the molecular mechanism of propofol in hepatic I/R injury has not been fully understood. Male Sprague-Dawley rats were randomly assigned into Sham group, hepatic I/R group, and propofol treatment group. I/R injury was attained by ischemia for 1 h and reperfusion for 2 h. Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activity were detected. QSG-7701 cells were cultured in hypoxia condition for 15 h and then in reoxygenation condition for 6 h to imitate hypoxia/reoxygenation (H/R) injury in vitro. Real-time RT-PCR and Western blot were performed to determine the expression of miR-133a-5p and MAPK6. Luciferase reporter assay was used to determine the regulation of miR-133a-5p on MAPK6. Propofol significantly reduced the activities of serum AST and ALT induced by hepatic I/R injury in rats. Propofol increased the level of miR-133a-5p and decreased the expression of MAPK6 in vivo and in vitro. Luciferase reporter assay showed that MAPK6 was a target of miR-133a-5p. Knockdown of miR-133a-5p abrogated the effect of propofol on the upregulation of MAPK6 induced by H/R. MAPK6 overexpression promoted the cell apoptosis induced by H/R which could be attenuated by propofol. Finally, we found that miR-133a-5p reversed the protective effect of propofol in rats with hepatic I/R injury. Propofol showed protective roles for hepatic I/R injury in vivo and H/R injury in vitro, which involved with miR-133a-5p regulating the expression of MAPK6.

show abstract

Propofol Suppressed Hypoxia/Reoxygenation‐Induced Apoptosis in HBVSMC by Regulation of the Expression of Bcl‐2, Bax, Caspase3, Kir6.1, and p‐JNK

Cited by 34 publications

References 50 publications

Tetrahydroxystilbene Glucoside Ameliorates Infrasound-Induced Central Nervous System (CNS) Injury by Improving Antioxidant and Anti-Inflammatory Capacity

Tetrahydroxystilbene Glucoside Ameliorates Infrasound-Induced Central Nervous System (CNS) Injury by Improving Antioxidant and Anti-Inflammatory Capacity

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

Propofol protects against hepatic ischemia/reperfusion injury via miR‐133a‐5p regulating the expression of MAPK6

Contact Info

Product

Resources

About