Neuroprotective effect of modified Wu-Zi-Yan-Zong granule, a traditional Chinese herbal medicine, on CoCl2-induced PC12 cells

Zeng, Ke‐Wu; Wang, Xuemei; Ko, Hyeonseok; Yang, Hyun Ok

doi:10.1016/j.jep.2010.03.018

Cited by 16 publications

(3 citation statements)

References 16 publications

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“…Then, 400 ll 19 binding buffer was added to each sample, and the fluorescein-5-isothiocyanate (FITC) and PI fluorescence were measured using flow cytometry through FL-1 filter (530 nm) and FL-2 filter (585 nm). Viable cells were annexin V negative and PI negative, early apoptotic cell were annexin V positive and PI negative, and late apoptotic cells or necrotic cells were annexin V positive and PI positive (Zeng et al 2010). …”

Section: Annexin V/pi Staining Testmentioning

confidence: 96%

Neuroprotective Effect of Crocin on Acrylamide-induced Cytotoxicity in PC12 cells

et al. 2011

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Acrylamide (ACR) is a potent neurotoxic in human and animal models. In this study, the effect of crocin, main constituent of Crocus sativus L. (Saffron) on ACR-induced cytotoxicity was evaluated using PC12 cells as a suitable in vitro model. The exposure of PC12 cells to ACR reduced cell viability, increased DNA fragmented cells and phosphatidylserine exposure, and elevated Bax/Bcl-2 ratio. Results showed that ACR increased intracellular reactive oxygen species (ROS) in cells and ROS played an important role in ACR cytotoxicity. The pretreatment of cells with 10-50 μM crocin before ACR treatment significantly attenuated ACR cytotoxicity in a dose-dependent manner. Crocin inhibited the downregulation of Bcl-2 and the upregulation of Bax and decreased apoptosis in treated cells. Also, crocin inhibited ROS generation in cells exposed to ACR. In conclusion, our results indicated that pretreatment with crocin protected cells from ACR-induced apoptosis partly by inhibition of intracellular ROS production.

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Section: Annexin V/pi Staining Testmentioning

confidence: 96%

Neuroprotective Effect of Crocin on Acrylamide-induced Cytotoxicity in PC12 cells

et al. 2011

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“…Treatment with 2ccPA suppressed the CoCl 2 -induced increase in the Bax/Bcl-2 ratio, which suggested that 2ccPA protected oligodendrocyte cells from CoCl 2 -induced mitochondrial apoptosis. In addition, we observed activation of p38MAPK and JNK during CoCl 2 -induced apoptosis [29, 30]. CoCl 2 increased the phosphorylation levels of p38MAPK and JNK protein, which were suppressed by 2ccPA treatment (Fig.…”

Section: Resultsmentioning

confidence: 95%

Protective and therapeutic role of 2-carba-cyclic phosphatidic acid in demyelinating disease

Yamamoto

Yamashina

Ishikawa

et al. 2017

J Neuroinflammation

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BackgroundMultiple sclerosis is a neuroinflammatory demyelinating and neurodegenerative disease of the central nervous system characterized by recurrent and progressive demyelination/remyelination cycles, neuroinflammation, oligodendrocyte loss, demyelination, and axonal degeneration. Cyclic phosphatidic acid (cPA) is a natural phospholipid mediator with a unique cyclic phosphate ring structure at the sn-2 and sn-3 positions of the glycerol backbone. We reported earlier that cPA elicits a neurotrophin-like action and protects hippocampal neurons from ischemia-induced delayed neuronal death. We designed, chemically synthesized, and metabolically stabilized derivatives of cPA: 2-carba-cPA (2ccPA), a synthesized compound in which one of the phosphate oxygen molecules is replaced with a methylene group at the sn-2 position. In the present study, we investigated whether 2ccPA exerts protective effects in oligodendrocytes and suppresses pathology in the two most common mouse models of multiple sclerosis.MethodsTo evaluate whether 2ccPA has potential beneficial effects on the pathology of multiple sclerosis, we investigated the effects of 2ccPA on oligodendrocyte cell death in vitro and administrated 2ccPA to mouse models of experimental autoimmune encephalomyelitis (EAE) and cuprizone-induced demyelination.ResultsWe demonstrated that 2ccPA suppressed the CoCl2-induced increase in the Bax/Bcl-2 protein expression ratio and phosphorylation levels of p38MAPK and JNK protein. 2ccPA treatment reduced cuprizone-induced demyelination, microglial activation, NLRP3 inflammasome, and motor dysfunction. Furthermore, 2ccPA treatment reduced autoreactive T cells and macrophages, spinal cord injury, and pathological scores in EAE, the autoimmune multiple sclerosis mouse model.ConclusionsWe demonstrated that 2ccPA protected oligodendrocytes via suppression of the mitochondrial apoptosis pathway. Also, we found beneficial effects of 2ccPA in the multiperiod of cuprizone-induced demyelination and the pathology of EAE. These data indicate that 2ccPA may be a promising compound for the development of new drugs to treat demyelinating disease and ameliorate the symptoms of multiple sclerosis.

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“…The current results further showed that the protective effect of Rb1 in RGC-5 cell injury induced by CoCl 2 was exerted primarily against early apoptotic cells. The recent studies showed that CoCl 2 induced apoptosis through the activation of caspase-3 in in vitro studies (16,17). The study by Kong et al revealed that Rb1 decreased the expression of caspase-3 (11).…”

Section: Discussionmentioning

confidence: 99%

Ginsenoside Rb1 protects rat retinal ganglion cells against hypoxia and oxidative stress

Liu

Chen

Huang

et al. 2013

Molecular Medicine Reports

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The current study was designed to investigate the effect of ginsenoside Rb1 (Rb1) on apoptosis induced by hypoxia and oxidative stress in a retinal ganglion cell line (RGC-5). The underlying mechanism was also investigated. RGC-5 cells were pretreated with 10 µmol/l Rb1 for 24 h and exposed to 400 µmol/l cobalt chloride (CoCl2) for 48 h or 600 µmol/l H2O2 for 24 h. The percentage of cells actively undergoing apoptosis was determined by ﬂow cytometry with Annexin V/propidium iodide (PI) double staining. The expression of caspases was determined using western blot analysis. CoCl2 and H2O2 treatments significantly increased the apoptotic percentages to 24.5 and 21.63%, respectively. Pretreatment of Rb1 reduced the total apoptotic percentages to 15.12 and 12.03%, respectively. The expression of cleaved caspase-3, -9 and -8 was increased in the CoCl2-treated group, however, caspase-3 was not increased in the H2O2-treated group. Pretreatment of Rb1 reduced the expression of cleaved caspase-3 and -9 in the CoCl2-treated group, but reduced only cleaved caspase-9 in the H2O2-treated group. These results suggest that Rb1 may prevent RGC-5 cells from apoptosis against hypoxia and oxidative stress via the mitochondrial pathway.

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Neuroprotective effect of modified Wu-Zi-Yan-Zong granule, a traditional Chinese herbal medicine, on CoCl2-induced PC12 cells

Cited by 16 publications

References 16 publications

Neuroprotective Effect of Crocin on Acrylamide-induced Cytotoxicity in PC12 cells

Neuroprotective Effect of Crocin on Acrylamide-induced Cytotoxicity in PC12 cells

Protective and therapeutic role of 2-carba-cyclic phosphatidic acid in demyelinating disease

Ginsenoside Rb1 protects rat retinal ganglion cells against hypoxia and oxidative stress

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