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MnTMPyP, a cell-permeant SOD mimetic, reduces oxidative stress and apoptosis following renal ischemia-reperfusion.
Am J Physiol Renal Physiol. 2009 Feb; 296(2):F266-76.AJ

Abstract

Oxidative stress and apoptosis are important factors in the etiology of renal ischemia-reperfusion (I/R) injury. The present study tested the hypothesis that the cell-permeant SOD mimetic manganese(III) tetrakis(1-methyl-4-pyridyl)porphyrin (MnTMPyP) protects the kidney from I/R-mediated oxidative stress and apoptosis in vivo. Male Sprague-Dawley rats (175-220 g) underwent renal I/R by bilateral clamping of the renal arteries for 45 min followed by reperfusion for 24 h. To examine the role of reactive oxygen species (ROS) in renal I/R injury, a subset of animals were treated with either saline vehicle (I/R Veh) or MnTMPyP (I/R Mn) (5 mg/kg ip) 30 min before and 6 h after surgery. MnTMPyP significantly attenuated the I/R-mediated increase in serum creatinine levels and decreased tubular epithelial cell damage following I/R. MnTMPyP also decreased TNF-alpha levels, gp(91phox), and lipid peroxidation after I/R. Furthermore, MnTMPyP inhibited the I/R-mediated increase in apoptosis and caspase-3 activation. Interestingly, although MnTMPyP did not increase expression of the antiapoptotic protein Bcl-2, it decreased the expression of the proapoptotic genes Bax and FasL. These results suggest that MnTMPyP is effective in reducing apoptosis associated with renal I/R injury and that multiple signaling mechanisms are involved in ROS-mediated cell death following renal I/R injury.

Authors+Show Affiliations

Division of Transplant Surgery, Medical College of Wisconsin, 8701 Watertown Plank Rd., Milwaukee, WI 53226, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

19091787

Citation

Liang, Huan Ling, et al. "MnTMPyP, a Cell-permeant SOD Mimetic, Reduces Oxidative Stress and Apoptosis Following Renal Ischemia-reperfusion." American Journal of Physiology. Renal Physiology, vol. 296, no. 2, 2009, pp. F266-76.
Liang HL, Hilton G, Mortensen J, et al. MnTMPyP, a cell-permeant SOD mimetic, reduces oxidative stress and apoptosis following renal ischemia-reperfusion. Am J Physiol Renal Physiol. 2009;296(2):F266-76.
Liang, H. L., Hilton, G., Mortensen, J., Regner, K., Johnson, C. P., & Nilakantan, V. (2009). MnTMPyP, a cell-permeant SOD mimetic, reduces oxidative stress and apoptosis following renal ischemia-reperfusion. American Journal of Physiology. Renal Physiology, 296(2), F266-76. https://doi.org/10.1152/ajprenal.90533.2008
Liang HL, et al. MnTMPyP, a Cell-permeant SOD Mimetic, Reduces Oxidative Stress and Apoptosis Following Renal Ischemia-reperfusion. Am J Physiol Renal Physiol. 2009;296(2):F266-76. PubMed PMID: 19091787.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - MnTMPyP, a cell-permeant SOD mimetic, reduces oxidative stress and apoptosis following renal ischemia-reperfusion. AU - Liang,Huan Ling, AU - Hilton,Gail, AU - Mortensen,Jordan, AU - Regner,Kevin, AU - Johnson,Christopher P, AU - Nilakantan,Vani, Y1 - 2008/12/17/ PY - 2008/12/19/entrez PY - 2008/12/19/pubmed PY - 2009/3/31/medline SP - F266 EP - 76 JF - American journal of physiology. Renal physiology JO - Am J Physiol Renal Physiol VL - 296 IS - 2 N2 - Oxidative stress and apoptosis are important factors in the etiology of renal ischemia-reperfusion (I/R) injury. The present study tested the hypothesis that the cell-permeant SOD mimetic manganese(III) tetrakis(1-methyl-4-pyridyl)porphyrin (MnTMPyP) protects the kidney from I/R-mediated oxidative stress and apoptosis in vivo. Male Sprague-Dawley rats (175-220 g) underwent renal I/R by bilateral clamping of the renal arteries for 45 min followed by reperfusion for 24 h. To examine the role of reactive oxygen species (ROS) in renal I/R injury, a subset of animals were treated with either saline vehicle (I/R Veh) or MnTMPyP (I/R Mn) (5 mg/kg ip) 30 min before and 6 h after surgery. MnTMPyP significantly attenuated the I/R-mediated increase in serum creatinine levels and decreased tubular epithelial cell damage following I/R. MnTMPyP also decreased TNF-alpha levels, gp(91phox), and lipid peroxidation after I/R. Furthermore, MnTMPyP inhibited the I/R-mediated increase in apoptosis and caspase-3 activation. Interestingly, although MnTMPyP did not increase expression of the antiapoptotic protein Bcl-2, it decreased the expression of the proapoptotic genes Bax and FasL. These results suggest that MnTMPyP is effective in reducing apoptosis associated with renal I/R injury and that multiple signaling mechanisms are involved in ROS-mediated cell death following renal I/R injury. SN - 1931-857X UR - https://www.unboundmedicine.com/medline/citation/19091787/MnTMPyP_a_cell_permeant_SOD_mimetic_reduces_oxidative_stress_and_apoptosis_following_renal_ischemia_reperfusion_ L2 - https://journals.physiology.org/doi/10.1152/ajprenal.90533.2008?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -