ArticleScientific reports2019
Mn-TAT PTD-Ngb attenuates oxidative injury by an enhanced ROS scavenging ability and the regulation of redox signaling pathway.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 15 citations in OpenAlex.
- Oxidized Mitochondrial DNA Engages TLR9 to Activate the NLRP3 Inflammasome in Myelodysplastic Syndromes.International journal of molecular sciences · 2023Article
- NLRP3 inflammasome activation in response to metals.Frontiers in immunology · 2023Review
- New Strategies for Stroke Therapy: Nanoencapsulated Neuroglobin.Pharmaceutics · 2022Review
- Asafoetida exerts neuroprotective effect on oxidative stress induced apoptosis through PI3K/Akt/GSK3β/Nrf2/HO-1 pathway.Chinese medicine · 2022Article
- Role of Neuroglobin in the Neuroprotective Actions of Estradiol and Estrogenic Compounds.Cells · 2021Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
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Abstract
Neurological diseases have a close relationship to excessive reactive oxygen species (ROS). Neuroglobin (Ngb), an intrinsic protective factor, protected cells from hypoxic/ischemic injury. In the present, we reported a novel neuroprotective manganese porphyrin reconstituted metal protein, Mn-TAT PTD-Ngb, consisting of a HIV Tat protein transduction domain sequence (TAT PTD) attached to the N-terminal of apo-Ngb. Mn-TAT PTD-Ngb had a stronger ROS scavenging ability than that of TAT PTD-Ngb, and reduced intracellular ROS production and restored the function of the mitochondria and inhibited the mitochondria-dependent apoptosis. Besides, Mn-TAT PTD-Ngb activated the phosphoinositide-3 kinase (PI3K)/Akt signaling pathway, which up-regulated the expression of nuclear factor E2-related factor 2 (Nrf2), Heme oxygenase-1 (HO-1), superoxide dismutase (SOD), catalase (CAT). The results showed that the redox chemistry of Mn-TAT PTD-Ngb and redox regulation of multiple signaling pathways attenuated the oxidative injury.
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