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MnTMPyP inhibits paraquat-induced pulmonary epithelial-like cell injury by inhibiting oxidative stress.
J Toxicol Sci. 2018; 43(9):545-555.JT

Abstract

OBJECTIVE

To investigate the protective effect and underlying mechanism of the superoxide dismutase mimic, manganese (III) tetrakis (1-methyl-4-pyridyl) porphyrin pentachloride (MnTMPyP), on paraquat (PQ)-induced lung alveolar epithelial-like cell injury.

METHODS

Lung alveolar epithelial-like cells (A549) were pretreated with 10 μM MnTMPyP for 1.5 hr and then cultured with or without PQ (750 uM) for 24 hr. Cell survival was determined using the MTT assay. Apoptosis, mitochondrial transmembrane potential, reactive oxygen species (ROS) production, and Ca2+ levels were measured using flow cytometry. Glutathione reductase activity (GR activity) and caspase-3 activation were determined using spectrophotometry. Expression of the apoptosis proteins, Bcl-2 and Bax, and the endoplasmic reticulum (ER) stress proteins, glucose regulatory protein 78 (Grp78) and C/EBP homologous protein (CHOP), was measured using Western blot analysis.

RESULTS

Cell viability, mitochondrial membrane potential, GR activity, and Bcl-2 expression were decreased, but apoptosis, ROS production, caspase-3 activity, cytoplasmic Ca2+ levels, and Bax, Grp78 and CHOP expression were all increased in the PQ group compared to the control group. There were no statistically significant changes in the MnTMPyP group. Cell viability, GR activity, mitochondrial membrane potential, and Bcl-2 protein expression were all increased, while apoptosis, ROS production, cytoplasmic Ca2+ levels, caspase-3 activity, and Bax, Grp78 and CHOP expression were all significantly reduced in the MnTMPyP group compared to PQ group.

CONCLUSION

MnTMPyP effectively reduced PQ-induced lung epithelial-like cell injury, and the underlying mechanism is related to antagonism of PQ-induced oxidative stress.

Authors+Show Affiliations

Department of Emergency, the First Hospital, China Medical University, China.Department of Emergency, the First Hospital, China Medical University, China.Department of Emergency, the First Hospital, China Medical University, China.Department of Emergency, the First Hospital, China Medical University, China.Department of Emergency, the First Hospital, China Medical University, China.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

30185695

Citation

Xu, Yongmin, et al. "MnTMPyP Inhibits Paraquat-induced Pulmonary Epithelial-like Cell Injury By Inhibiting Oxidative Stress." The Journal of Toxicological Sciences, vol. 43, no. 9, 2018, pp. 545-555.
Xu Y, Sun D, Song C, et al. MnTMPyP inhibits paraquat-induced pulmonary epithelial-like cell injury by inhibiting oxidative stress. J Toxicol Sci. 2018;43(9):545-555.
Xu, Y., Sun, D., Song, C., Wang, R., & Dong, X. (2018). MnTMPyP inhibits paraquat-induced pulmonary epithelial-like cell injury by inhibiting oxidative stress. The Journal of Toxicological Sciences, 43(9), 545-555. https://doi.org/10.2131/jts.43.545
Xu Y, et al. MnTMPyP Inhibits Paraquat-induced Pulmonary Epithelial-like Cell Injury By Inhibiting Oxidative Stress. J Toxicol Sci. 2018;43(9):545-555. PubMed PMID: 30185695.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - MnTMPyP inhibits paraquat-induced pulmonary epithelial-like cell injury by inhibiting oxidative stress. AU - Xu,Yongmin, AU - Sun,Dazhuang, AU - Song,Chunqing, AU - Wang,Rui, AU - Dong,Xuesong, PY - 2018/9/7/entrez PY - 2018/9/7/pubmed PY - 2018/10/13/medline KW - Apoptosis KW - Lung alveolar epithelial cell KW - MnTMPyP KW - Oxidative stress KW - Paraquat SP - 545 EP - 555 JF - The Journal of toxicological sciences JO - J Toxicol Sci VL - 43 IS - 9 N2 - OBJECTIVE: To investigate the protective effect and underlying mechanism of the superoxide dismutase mimic, manganese (III) tetrakis (1-methyl-4-pyridyl) porphyrin pentachloride (MnTMPyP), on paraquat (PQ)-induced lung alveolar epithelial-like cell injury. METHODS: Lung alveolar epithelial-like cells (A549) were pretreated with 10 μM MnTMPyP for 1.5 hr and then cultured with or without PQ (750 uM) for 24 hr. Cell survival was determined using the MTT assay. Apoptosis, mitochondrial transmembrane potential, reactive oxygen species (ROS) production, and Ca2+ levels were measured using flow cytometry. Glutathione reductase activity (GR activity) and caspase-3 activation were determined using spectrophotometry. Expression of the apoptosis proteins, Bcl-2 and Bax, and the endoplasmic reticulum (ER) stress proteins, glucose regulatory protein 78 (Grp78) and C/EBP homologous protein (CHOP), was measured using Western blot analysis. RESULTS: Cell viability, mitochondrial membrane potential, GR activity, and Bcl-2 expression were decreased, but apoptosis, ROS production, caspase-3 activity, cytoplasmic Ca2+ levels, and Bax, Grp78 and CHOP expression were all increased in the PQ group compared to the control group. There were no statistically significant changes in the MnTMPyP group. Cell viability, GR activity, mitochondrial membrane potential, and Bcl-2 protein expression were all increased, while apoptosis, ROS production, cytoplasmic Ca2+ levels, caspase-3 activity, and Bax, Grp78 and CHOP expression were all significantly reduced in the MnTMPyP group compared to PQ group. CONCLUSION: MnTMPyP effectively reduced PQ-induced lung epithelial-like cell injury, and the underlying mechanism is related to antagonism of PQ-induced oxidative stress. SN - 1880-3989 UR - https://www.unboundmedicine.com/medline/citation/30185695/MnTMPyP_inhibits_paraquat_induced_pulmonary_epithelial_like_cell_injury_by_inhibiting_oxidative_stress_ L2 - https://dx.doi.org/10.2131/jts.43.545 DB - PRIME DP - Unbound Medicine ER -