Umbilical cord-derived mesenchymal stem cell conditioned medium reverses neuronal oxidative injury by inhibition of TRPM2 activation and the JNK signaling pathway
- Mol Biol Rep. 2022 Aug;49(8):7337-7345. doi: 10.1007/s11033-022-07524-9.
- 1. Key Laboratory of Ningxia Stem Cell and Regenerative Medicine, General Hospital of Ningxia Medical University, 750001, Yinchuan, China.
- 2. Ningxia Key Laboratory of Cerebrocranial Diseases, Ningxia Medical University, 750004, Yinchuan, China.
- 3. School of Pharmacology, Ningxia Medical University, 750004, Yinchuan, China. [email protected].
- 4. Ningxia Key Laboratory of Cerebrocranial Diseases, Ningxia Medical University, 750004, Yinchuan, China. [email protected].
- 5. Key Laboratory of Ningxia Stem Cell and Regenerative Medicine, General Hospital of Ningxia Medical University, 750001, Yinchuan, China. [email protected].
Background: The mechanism by which MSC-CM protects neuronal cells against ischemic injury remains to be elucidated. In this study, we aimed to clarify the protective effect of umbilical cord-derived mesenchymal stem cell conditioned medium (UC-MSC-CM) on neuronal oxidative injury and its potential mechanism.
Methods and results: Neuronal oxidative damage was mimicked by H2O2 treatment of the HT22 cell line. The numbers of cleaved-Caspase-3-positive cells and protein expression of Caspase-9 induced by H2O2 treatment were decreased by UC-MSC-CM treatment. Furthermore, SOD protein expression was increased in the MSC-CM group compared with that in the H2O2 group. The H2O2-induced TRPM2-like currents in HT22 cells were attenuated by MSC-CM treatment. In addition, H2O2 treatment downregulated the expression of p-JNK protein in HT22 cells, and this the downward trend was reversed by incubation with MSC-CM.
Conclusions: UC-MSC-CM protects neurons against oxidative injury, possibly by inhibiting activation of TRPM2 and the JNK signaling pathway.