مرکز اطلاعات علمی Scientific Information Database (SID) - Trusted Source for Research and Academic Resources

video

مرکز اطلاعات علمی Scientific Information Database (SID) - Trusted Source for Research and Academic Resources

sound

مرکز اطلاعات علمی Scientific Information Database (SID) - Trusted Source for Research and Academic Resources

Persian Version

مرکز اطلاعات علمی Scientific Information Database (SID) - Trusted Source for Research and Academic Resources

View:

165
مرکز اطلاعات علمی Scientific Information Database (SID) - Trusted Source for Research and Academic Resources

Download:

121
مرکز اطلاعات علمی Scientific Information Database (SID) - Trusted Source for Research and Academic Resources

Cites:

1

Information Journal Paper

Title

Adrenomedullin protects rat dorsal root ganglion neurons against doxorubicin-induced toxicity by ameliorating oxidative stress

Pages

  1197-1206

Abstract

 Objective(s): Despite effective anticancer effects, the use of Doxorubicin (DOX) is hindered due to its cardio and neurotoxicity. The neuroprotective effect of Adrenomedullin (AM) was shown in several studies. The present study aimed to evaluate the possible protective effects of AM against DOX-induced toxicity in Dorsal root ganglia (DRGs) neurons. Materials and Methods: Rat embryonic DRG neurons were isolated and cultured. The effect of various concentrations of DOX (0. 0 to 100 μ M) in the absence or presence of AM (3. 125-100 nM) on cell death, apoptosis, Oxidative stress, expression of tumor necrosis-α (TNF-α ), interleukin1-β (IL-1β ), inducible nitric oxide synthase (iNOS), matrix metalloproteinase (MMP) 3 and 13, and SRY-related protein 9 (SOX9) were examined. Results: Based on MTT assay data, DOX decreased the viability of DRG neurons in a dose and timedependent manner (IC50=6. 88 μ m) while dose-dependently, AM protected DRG neurons against DOXinduced cell death. Furthermore, results of annexin V apoptosis assay revealed the protective effects of AM (25 nm) against DOX (6. 88 μ M)-induced apoptosis and necrosis of DRG neurons. Also, AM significantly ameliorated DOX-induced Oxidative stress in DRG neurons. Real-time PCR results showed a significant increase in the expression of TNF-α , IL-1β , iNOS, MMP 3, and MMP 13, and a decrease in the expression of SOX9 following treatment with DOX. Treatment with AM (25 nM) significantly reversed the effects of DOX on the above-mentioned genes expression. Conclusion: Our findings suggest that AM can be considered a novel ameliorating drug against DOXinduced neurotoxicity.

Cites

References

  • No record.
  • Cite

    APA: Copy

    Mahmoodazdeh, Amir, Shafiee, Sayed Mohammad, Sisakht, Mohsen, Khoshdel, Zahra, & TAKHSHID, MOHAMMAD ALI. (2020). Adrenomedullin protects rat dorsal root ganglion neurons against doxorubicin-induced toxicity by ameliorating oxidative stress. IRANIAN JOURNAL OF BASIC MEDICAL SCIENCES, 23(9), 1197-1206. SID. https://sid.ir/paper/747925/en

    Vancouver: Copy

    Mahmoodazdeh Amir, Shafiee Sayed Mohammad, Sisakht Mohsen, Khoshdel Zahra, TAKHSHID MOHAMMAD ALI. Adrenomedullin protects rat dorsal root ganglion neurons against doxorubicin-induced toxicity by ameliorating oxidative stress. IRANIAN JOURNAL OF BASIC MEDICAL SCIENCES[Internet]. 2020;23(9):1197-1206. Available from: https://sid.ir/paper/747925/en

    IEEE: Copy

    Amir Mahmoodazdeh, Sayed Mohammad Shafiee, Mohsen Sisakht, Zahra Khoshdel, and MOHAMMAD ALI TAKHSHID, “Adrenomedullin protects rat dorsal root ganglion neurons against doxorubicin-induced toxicity by ameliorating oxidative stress,” IRANIAN JOURNAL OF BASIC MEDICAL SCIENCES, vol. 23, no. 9, pp. 1197–1206, 2020, [Online]. Available: https://sid.ir/paper/747925/en

    Related Journal Papers

  • No record.
  • Related Seminar Papers

  • No record.
  • Related Plans

  • No record.
  • Recommended Workshops






    Move to top
    telegram sharing button
    whatsapp sharing button
    linkedin sharing button
    twitter sharing button
    email sharing button
    email sharing button
    email sharing button
    sharethis sharing button