- 作者: Lei Li, Hong-kun Jiang , Yun-peng Li, Yan-ping Guo
- 作者服務機構: Department of Orthopedics, Shengjing Hospital of China Medical University, Shenyang , China
- 中文摘要: --
- 英文摘要:
Background:
Hydrogen sulfide (H2S), a novel gaseous mediator, has been recognized as an important neuromodulator and neuroprotective agent in the nervous system. The present study was undertaken to study the effects of exogenous
H2S on ischemia/reperfusion (I/R) injury of spinal cord and the underlying mechanisms.
Methods:
The effects of exogenous H2S on I/R injury were examined by using assessment of hind motor function, spinal cord infarct zone by Triphenyltetrazolium chloride (TTC) staining. Autophagy was evaluated by expressions of
Microtubule associated protein 1 light chain 3 (LC3) and Beclin-1 which were determined by using Quantitative Real-Time PCR and Western blotting, respectively.
Results:
Compared to I/R injury groups, H2S pretreatment had reduced spinal cord infarct zone, improved hind motor function in rats. Quantitative Real-Time PCR or Western blotting results showed that H2S pretreatment also
downregulated miR-30c expression and upregulated Beclin-1 and LC3II expression in spinal cord. In vitro, miR-30c was showed to exert negative effect on Beclin-1 expression by targeting its 3’UTR in SY-SH-5Y cells treated with Oxygen, Glucose Deprivation (OGD). In rat model of I/R injury, pretreatment of pre-miR-30c or 3-MA (an inhibitor for autophagy) can abrogated spinal cord protective effect of H2S.
Conclusion:
H2S protects spinal cord and induces autophagy via miR-30c in a rat model of spinal cord hemia-reperfusion injury. - 中文關鍵字: --
- 英文關鍵字: Autophagy; Beclin-1; miR-30c; Microtubule associated protein 1 light chain 3 (LC3); Oxygen glucose deprivation (OGD)