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May-2015 Volume 9 Issue 5

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Article

Neuroprotective effect of paeoniflorin on H2O2-induced apoptosis in PC12 cells by modulation of reactive oxygen species and the inflammatory response

  • Authors:
    • Peng Li
    • Zhaohui Li
  • View Affiliations / Copyright

    Affiliations: Medical College of Nankai University, Tianjin 300071, P.R. China, Department of Ophthalmology, General Hospital of PLA, Beijing 100853, P.R. China
  • Pages: 1768-1772
    |
    Published online on: March 16, 2015
       https://doi.org/10.3892/etm.2015.2360
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Abstract

Paeoniflorin (PF) is a product derived from Paeoniae Radix and is commonly prescribed in traditional Chinese medicine. PF has been reported to exhibit neuroprotective, anti‑ischemic, antioxidant, anti‑inflammatory and anticancer effects. The neuroprotective properties of PF have been demonstrated in animal models of various neuropathologies. The present study investigated the effects of PF on hydrogen peroxide (H2O2)‑induced apoptosis in PC12 cells, to improve the understanding of the mechanisms underlying its neuroprotective properties. The H2O2‑induced apoptosis of PC12 cells resulted in a reduction in the B‑cell lymphoma 2 (Bcl‑2)/Bcl‑2‑associated X protein ratio and the activation of caspase‑3. PF treatment was observed to reverse the apoptotic process and to modulate the expression levels of a number of apoptosis‑associated proteins. Furthermore, PF significantly mitigated the H2O2‑induced reduction in cell viability, in addition to scavenging reactive oxygen species and preventing the release of lactate dehydrogenase from the PC12 cells. In addition, the apoptosis‑associated activation of nuclear factor (NF)‑κB was inhibited in the PF‑treated cells, and the expression levels of tumor necrosis factor α and interleukin (IL)‑1β were reduced. In conclusion, the present study demonstrated that PF was able to reduce H2O2‑induced toxicity by blocking the activation of the neuroinflammatory factor NF‑κB. These results suggest that PF may be a valuable neuroprotective agent for the treatment of neurological disease and injury.
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Copy and paste a formatted citation
Spandidos Publications style
Li P and Li Z: Neuroprotective effect of paeoniflorin on H2O2-induced apoptosis in PC12 cells by modulation of reactive oxygen species and the inflammatory response. Exp Ther Med 9: 1768-1772, 2015.
APA
Li, P., & Li, Z. (2015). Neuroprotective effect of paeoniflorin on H2O2-induced apoptosis in PC12 cells by modulation of reactive oxygen species and the inflammatory response. Experimental and Therapeutic Medicine, 9, 1768-1772. https://doi.org/10.3892/etm.2015.2360
MLA
Li, P., Li, Z."Neuroprotective effect of paeoniflorin on H2O2-induced apoptosis in PC12 cells by modulation of reactive oxygen species and the inflammatory response". Experimental and Therapeutic Medicine 9.5 (2015): 1768-1772.
Chicago
Li, P., Li, Z."Neuroprotective effect of paeoniflorin on H2O2-induced apoptosis in PC12 cells by modulation of reactive oxygen species and the inflammatory response". Experimental and Therapeutic Medicine 9, no. 5 (2015): 1768-1772. https://doi.org/10.3892/etm.2015.2360
Copy and paste a formatted citation
x
Spandidos Publications style
Li P and Li Z: Neuroprotective effect of paeoniflorin on H2O2-induced apoptosis in PC12 cells by modulation of reactive oxygen species and the inflammatory response. Exp Ther Med 9: 1768-1772, 2015.
APA
Li, P., & Li, Z. (2015). Neuroprotective effect of paeoniflorin on H2O2-induced apoptosis in PC12 cells by modulation of reactive oxygen species and the inflammatory response. Experimental and Therapeutic Medicine, 9, 1768-1772. https://doi.org/10.3892/etm.2015.2360
MLA
Li, P., Li, Z."Neuroprotective effect of paeoniflorin on H2O2-induced apoptosis in PC12 cells by modulation of reactive oxygen species and the inflammatory response". Experimental and Therapeutic Medicine 9.5 (2015): 1768-1772.
Chicago
Li, P., Li, Z."Neuroprotective effect of paeoniflorin on H2O2-induced apoptosis in PC12 cells by modulation of reactive oxygen species and the inflammatory response". Experimental and Therapeutic Medicine 9, no. 5 (2015): 1768-1772. https://doi.org/10.3892/etm.2015.2360
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