The post‐therapeutic effect of rapamycin in mild traumatic brain‐injured rats ensuing in the upregulation of autophagy and mitophagy
Abstract
Mild traumatic brain injury (mTBI), common in juveniles, has been reported to be caused by sports‐related concussion. Many young children may suffer from post‐concussion syndrome. mTBI, in early stages of life, could play a part in neuron apoptosis and degeneration, cognitive and motor coordination impairment, as well as dementia. Our study was aimed at further investigating the post‐therapeutic efficacy of rapamycin in the recuperation of mTBI while at the same time investigating the metamorphosis in both autophagy and mitophagy in mTBI. We created a weight‐drop rat mTBI model with the administration of rapamycin at 4 h after every mTBI. Behavioral tests of beam walking and open field task indicated the expected improvement of cognitive and motor coordination functions. Both Western blot and immunofluorescence examinations revealed increased Beclin‐1 and PINK1 in the treated rats as well as reduction of caspase‐3 and cytochrome C (Cyt C). More so, the TUNEL staining evidenced curtailment of apoptotic cells following treatment with rapamycin. The upregulation of Beclin‐1 and PINK1 and the downregulation of caspase‐3 and Cyt C extrapolate that rapamycin plays neuroprotective as well as anti‐apoptotic role via interposition of both autophagy and mitophagy.
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Rapamycin promotes autophagosome formation and induces mitophagy by upregulating the parkin/PINK1 pathway.
“rapamycin, which promotes autophagosome formation30, and was shown to induce mitophagy by upregulating the parkin/PINK1 pathway25,40–42.”
From Altered mitochondrial dynamics and function in APOE4-expressing astrocytes (2020) · cites this paper as [42]
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Cargo recognition failure is responsible for inefficient autophagy in Huntington’s disease
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Altered mitochondrial dynamics and function in APOE4-expressing astrocytes
Schmukler, E., Solomon, S., Simonovitch, S., Goldshmit, Y., Wolfson, E., Michaelson, D. M., & Pinkas-Kramarski, R. (2020) · Cell Death & Disease · doi:10.1038/s41419-020-02776-4 · Cited by 125 · see citing works
- Authors
- Wang, C., Hu, Z., Zou, Y., Xiang, M., Jiang, Y., Botchway, B. O. A., Huo, X., Du, X., & Fang, M.
- Affiliations
- Zhejiang Chinese Medical University (CN)
- Hangzhou Red Cross Hospital (CN)
- Zhejiang University (CN)
- Corresponding author
- Fang, Marong
- ORCID
- Venue
- Cell Biology International
- Publisher
- Wiley
- Published
- 2017-07-31
- Volume
- 41
- Issue
- 9
- Pages
- 1039-1047
- ISSN
- 1065-6995 (ISSN-L)
- 1095-8355
- OpenAlex
- W2732634470
- Cited by
- 39
- References
- 3
- Citations by year
- 2026: 4 · 2025: 2 · 2024: 5 · 2023: 5 · 2022: 1 · 2021: 4 · 2020: 6 · 2019: 7 · 2018: 4 · 2017: 1
- FWCI
- 3.35
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Cell Biology International (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (81671138, 81371493)
- Topics
- Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Health Sciences › Medicine › Epidemiology › Traumatic Brain Injury Research
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Keywords
- mild traumatic brain injury, rapamycin, autophagy, mitophagy, neuroprotection, apoptosis, Beclin-1, PINK1, caspase-3, cytochrome c, post-concussion syndrome, sports-related concussion, weight-drop injury model
- MeSH terms
- Animals, Autophagy, Brain Concussion, Disease Models, Animal, Male, Up-Regulation, Rats, Sprague-Dawley, Apoptosis, Neuroprotective Agents, Sirolimus, Rats, Mitophagy
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