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. Author manuscript; available in PMC: 2019 Nov 1.
Published in final edited form as: Food Chem Toxicol. 2018 Sep 8;121:387–395. doi: 10.1016/j.fct.2018.09.009

Figure 5. Permethrin induced phosphorylation (activation) of ERK1/2 via mGluR-PLC-PKC dependent pathway.

Figure 5.

Effects of bisindolylmaleimide I (a PKC antagonist, A), U-73122 (a PLC antagonist, B), and PHCCC (a group I mGluR antagonist, C) on permethrin’s effect on ERK1/2 activation. (D) Effect of group I mGluR agonists on ERK1/2 activation. Cells were treated with or without antagonist for 1 h before permethrin treatment, then co-incubated with permethrin for 30 min (A-C). HepG2 cells were treated with 10 and 50µM of group I mGluR agonist (S)-3,5-DHPG for 30 min (D). Numbers are mean ± S.E.M. n=5. Means with different letters are statistically different at P < 0.05. ERK1/2: Extracellular signal-related kinase 1/2; mGluR: metabotropic glutamate receptor; PKC: protein kinase C; PLC: phosphoinositide phospholipase C; (S)-3,5-DHPG: (S)-3,5-Dihydroxyphenylglycine.