Protective Effects of Crataegus pinnatifida Extracts and Crataegolic Acid Against Neurotoxicity of Paraquat in PC12 Cells

The neuroprotective mechanisms of Crataegus pinnatifida extracts and crataegolic acid were studied using paraquat induced cytotoxicity in PC12 cells. C. pinnatifida extracts were prepared using hexane, ethyl acetate, and 95% ethanol. Additionally, crataegolic acid (also known as maslinic acid) was found in C. pinnatifida extracts. Assessment methods included the examinations of cytotoxicity, intracellular reactive oxygen species and calcium changes, activity of caspase-3 and α-synuclein, apoptotic cell death, and the expression levels of the B-cell lymphoma 2 (Bcl-2) and BCL2-associated X (Bax) proteins to investigate the neuroprotective mechanisms of C. pinnatifida extracts and its active component, crataegolic acid. The three extracts and crataegolic acid exhibited potent neuroprotective actions against paraquat induced PC12 cell apoptosis at 5–20µg/mL and 80–100µM concentrations, respectively. The key protective mechanisms included decreasing cell apoptosis, upregulating Bcl-2 protein levels, and downregulating Bax protein levels. The 95% ethanol extract also decreased paraquat induced reactive oxygen species production, calcium overloading, and caspase-3 and α-synuclein activities. The beneficial effects of these extracts could be explained by the active component, crataegolic acid that also inhibited paraquat-induced apoptosis through the suppression of reactive oxygen species generation and the caspase-3 signaling pathway.

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Reactive oxygen species-mediated caspase-3 pathway involved in cell apoptosis of Karenia mikimotoi induced by linoleic acid

Algal Research ◽

10.1016/j.algal.2018.10.013 ◽

2018 ◽

Vol 36 ◽

pp. 48-56 ◽

Cited By ~ 1

Author(s):

Meiaoxue Han ◽

Renjun Wang ◽

Ning Ding ◽

Xiuxia Liu ◽

Ningning Zheng ◽

...

Keyword(s):

Reactive Oxygen Species ◽

Linoleic Acid ◽

Cell Apoptosis ◽

Caspase 3 ◽

Reactive Oxygen ◽

Oxygen Species ◽

Karenia Mikimotoi

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MPTP-induced reactive oxygen species promote cell death through a gradual activation of caspase-3 without expression of GRP78/Bip as a preventive measure against ER stress in PC12 cells

Life Sciences ◽

10.1016/s0024-3205(03)00351-5 ◽

2003 ◽

Vol 73 (5) ◽

pp. 581-593 ◽

Cited By ~ 16

Author(s):

Koji Shimoke ◽

Motoshige Kudo ◽

Toshihiko Ikeuchi

Keyword(s):

Reactive Oxygen Species ◽

Cell Death ◽

Er Stress ◽

Pc12 Cells ◽

Caspase 3 ◽

Reactive Oxygen ◽

Preventive Measure ◽

Oxygen Species ◽

Promote Cell Death

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Effects of the combination of active component extracts from Astragalus membranaceus and Panax notoginseng on apoptosis, reactive oxygen species and mitochondrial membrane potential of PC12 cells with oxidative injury

Journal of Chinese Integrative Medicine ◽

10.3736/jcim20121009 ◽

2012 ◽

pp. 1127-1134 ◽

Cited By ~ 6

Author(s):

XP Huang

Keyword(s):

Reactive Oxygen Species ◽

Membrane Potential ◽

Pc12 Cells ◽

Mitochondrial Membrane Potential ◽

Mitochondrial Membrane ◽

Active Component ◽

Reactive Oxygen ◽

Panax Notoginseng ◽

Astragalus Membranaceus ◽

Oxygen Species

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Atractylenolide I alleviates ischemia/reperfusion injury by preserving mitochondrial function and inhibiting caspase-3 activity

Journal of International Medical Research ◽

10.1177/0300060521993315 ◽

2021 ◽

Vol 49 (2) ◽

pp. 030006052199331

Author(s):

Caiqin Sun ◽

Xuesong Zhang ◽

Fei Yu ◽

Chen Liu ◽

Fangbin Hu ◽

...

Keyword(s):

Reactive Oxygen Species ◽

Flow Cytometry ◽

Mitochondrial Function ◽

Caspase 3 ◽

Ischemia Reperfusion ◽

Reactive Oxygen ◽

B Cell Lymphoma ◽

Oxygen Species ◽

Atractylenolide I ◽

Hypoxia Reoxygenation

Objective Myocardial ischemia/reperfusion (I/R) injury causes various severe heart diseases, including myocardial infarction. This study aimed to determine the therapeutic effect of atractylenolide I (ATR-I), which is an active ingredient isolated from Atractylodes macrocephala, on myocardial I/R injury. Methods Male Sprague-Dawley rats were randomly allocated to the five following groups (nine rats/group): control, I/R, and I/R + ATR-I preconditioning (10, 50, and 250 µg). The effects of ATR-I on rats with I/R injury were verified in cardiomyocytes with hypoxia/reoxygenation. Production of reactive oxygen species was determined. The proliferative ability of cardiomyocytes was detected using the bromodeoxyuridine assay. Mitochondrial membrane potential was measured using flow cytometry. Cellular apoptosis was assessed by flow cytometry and the terminal dUTP‐digoxigenin nick end labeling assay. Results I/R and hypoxia/reoxygenation injury increased mitochondrial dysfunction and activated caspase-3 and Bax/B cell lymphoma 2 expression in vitro and in vivo. ATR-I pretreatment dose-dependently significantly attenuated myocardial apoptosis and suppressed oxidative stress as reflected by increased mitochondrial DNA copy number and superoxide dismutase activity, and decreased reactive oxygen species and Ca2+ content. Conclusion ATR-I protects against I/R injury by protecting mitochondrial function and inhibiting activation of caspase-3.

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B-cell lymphoma 2 inhibitor ABT-737 induces Beclin1- and reactive oxygen species-dependent autophagy in Adriamycin-resistant human hepatocellular carcinoma cells

Tumor Biology ◽

10.1177/1010428317695965 ◽

2017 ◽

Vol 39 (3) ◽

pp. 101042831769596 ◽

Cited By ~ 4

Author(s):

Xiaoxiao Yao ◽

Xiaoning Li ◽

Dan Zhang ◽

Yingjun Xie ◽

Baozhen Sun ◽

...

Keyword(s):

Hepatocellular Carcinoma ◽

Reactive Oxygen Species ◽

B Cell ◽

Cell Apoptosis ◽

Cell Lymphoma ◽

Reactive Oxygen ◽

B Cell Lymphoma ◽

Carcinoma Cells ◽

Oxygen Species ◽

Hepatocellular Carcinoma Cells

ABT-737, a B-cell lymphoma 2 homology 3 mimetic, not only induces cell apoptosis by inhibiting the interaction of B-cell lymphoma 2 and Bax but also induces cell autophagy by interrupting the interaction of B-cell lymphoma 2 and Beclin1. Several recent studies have reported that ABT-737 has antitumor efficacy in diverse cancers. However, another study showed that hepatocellular carcinoma cells with high B-cell lymphoma 2 expression were resistant to ABT-737 compared to hepatocellular carcinoma cells with low B-cell lymphoma 2 expression. It was also found that ABT-737-induced autophagy is crucial for drug resistance. Here, we observed that of B-cell lymphoma 2 expression in Adriamycin-resistant human hepatocellular carcinoma HepG2/ADM cells is higher than that in human hepatocellular carcinoma HepG2 cells. Therefore, we further confirmed the mechanism and effect of autophagy induced by ABT-737 on apoptosis in HepG2/ADM cells with high B-cell lymphoma 2 expression. Our results showed that ABT-737 induced apoptosis and autophagy in time- and dose-dependent manner in HepG2/ADM cells, and this ABT-737-induced autophagy was Beclin1-dependent. In addition, we demonstrated that ABT-737 induced reactive oxygen species-mediated autophagy, and the reactive oxygen species-inhibitor N-acetyl-l-cysteine suppressed the reactive oxygen species-induced autophagy and ABT-737-induced increase in HepG2/ADM cell apoptosis. Furthermore, autophagy inhibitors increased HepG2/ADM cell apoptosis. In conclusion, our study further confirms that Beclin1- and reactive oxygen species-dependent autophagy induced by ABT-737 also plays a protective function in HepG2/ADM cells, which show B-cell lymphoma 2 expression higher than that in HepG2 cells.

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