JOURNAL ARTICLE

Treatment with hydrogen sulfide attenuates sublesional skeletal deterioration following motor complete spinal cord injury in rats

X Yang, D Hao, H Zhang, B Liu, M Yang, B He
Osteoporosis International 2017, 28 (2): 687-695
27591786

Treatment with hydrogen sulfide mitigates spinal cord injury-induced sublesional bone loss, possibly through abating oxidative stress, suppressing MMP activity, and activating Wnt/β-catenin signaling.

INTRODUCTION: Spinal cord injury (SCI)-induced sublesional bone loss represents the most severe osteoporosis and is resistant to available treatments to data. The present study was undertaken to explore the therapeutic potential of hydrogen sulfide (H2 S) against osteoporosis in a rodent model of motor complete SCI.

METHODS: SCI was generated by surgical transaction of the cord at the T3-T4 levels in rats. Treatment with NaHS was initiated through intraperitoneal injection of 0.1 ml/kg/day of 0.28 mol/l NaHS from 12 h following the surgery and over 14 subsequent days.

RESULTS: H2 S levels in plasma of SCI rats were lower, which was restored by treatment with exogenous H2 S. Treatment of SCI rats with exogenous H2 S had no significant effect on body mass but increased bone mineral density in femurs and tibiae, increased BV/TV, Tb.Th, and Tb.N and reduced Tb.Sp in proximal tibiae, and increased mineral apposition rate (MAR), bone formation rate (BFR), and osteoblast surface and reduced eroded surface and osteoclast surface in proximal tibiae. More importantly, H2 S treatment led to a significant enhancement in ultimate load, stiffness, and energy to max force of femoral diaphysis. Treatment of SCI rats with exogenous H2 S reduced malondialdehyde (MDA) levels in serum and femurs, decreased hydroxyproline levels, suppressed activities of matrix metallopeptidase 9 (MMP9), and upregulated Wnt3a, Wnt6, Wnt10, and ctnnb1 expression in femurs.

CONCLUSION: Treatment with H2 S mitigates SCI-induced sublesional bone loss, possibly through abating oxidative stress, suppressing MMP activity, and activating Wnt/β-catenin signaling.

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