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. Author manuscript; available in PMC: 2022 Apr 11.
Published in final edited form as: Free Radic Biol Med. 2022 Feb 1;181:52–61. doi: 10.1016/j.freeradbiomed.2022.01.030

Fig. 4.

Fig. 4.

Metformin has no significant effect in daf-16- and lgg-1-deficient hSOD1 mutant C. elegcuis. (A, B) Survival curves for hSOD1G93A worms lacking daf-16 or lgg-1. Metformin did not prolong the lifespan of hSOD1G93A worms lacking the daf-16 or lgg-1 gene. (C, D) Motor neuron survival and morphology in daf-16 and lgg-1 knockout worms treated with metformin. Compared to hSOD1G93A worms, metformin did not alleviate the neurotoxicity (C) or defects in neuronal morphology (D) caused by hSOD1 mutation in hSOD1G93A worms lacking daf-16 and lgg-1. (E, F) Oxidative stress response in hSOD1G93A mutant daf-16 and lgg-1 knockout worms treated with metformin. Metformin did not prolong the lifespan of hSOD1G93A worms lacking the daf-16 or lgg-1 gene and exposed to paraquat. (G) Locomotor behavior in hSOD1G93A worms lacking daf-16 or lgg-1. Metformin had no significant effect on the locomotion of hSOD1G93A mutant daf-16 or lgg-1 knockout worms. (H) Western blot analysis of protein extracts from transgenic strains. hSOD1G93A protein level in hSOD1 mutant worms was not reduced by metformin treatment in the absence of the daf-16 or lgg-1 gene. N ~ 100 worms per condition from 3 independent experiments.