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Fig. 1 | Molecular Brain

Fig. 1

From: Bisperoxovanadium promotes motor neuron survival and neuromuscular innervation in amyotrophic lateral sclerosis

Fig. 1

Treatment with bpV(pic) spares MNs in both in vivo and in vitro models of ALS. A The treatment schedule and experimental design for in vivo therapy of mSOD1G93A ALS mice. B and D Ventral horn motor neurons were significantly less than wild-type (WT) mice at 90 days of age (p < 0.001). A late pre-symptomatic daily treatment schedule between days 70 and 90 of age enhanced the number of NeuN-positive motor neurons (p = 0.003) but did not significantly alter Iba-1-positive microglial reactivity (p = 0.701) in the ventral horn of the lumbar spinal cord in mSOD1G93A mice compared to vehicle-treated mice (C and D). E bpV(pic) improved morphology and significantly enhanced viability (p = 0.018) and reduced LDH release (p = 0.025) in 24-h serum-starved mSOD1G93A-expressing motor neuron cells. F) In addition, bpV(pic) significantly increased p-AktS473/Akt ratio following treatment (p < 0.05) while co-culture with LY294002 under starvation conditions blocked bpV(pic)’s stimulating effects (p < 0.01). G & H) Gastrocnemius muscle assessment showed NMJs were innervated significantly more in bpV(pic)-treated mice than vehicle control mice (p = 0.018), but the treatment did not significantly affect muscle size and weight. ALS amyotrophic lateral sclerosis (ALS); NeuN neuronal nuclear antigen; mSOD1G93A Mutant superoxide dismutase 1 G93A; LDH lactate dehydrogenase; NMJ neuromuscular junction. WT group, n = 6; vehicle and bpV(pic) groups, n = 7 each). Scale bars = 250 μM (B and C) and 50 μM (H). All cell culture experiment data are from experiments performed in triplicate

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