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. 2019 Jan 7;9:1510. doi: 10.3389/fphar.2018.01510

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Copyright © 2019 Zhang, Cao, Lai, Xie and Zeng.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Puerarin inhibits Na_v1.8 in a neuropathic pain state may by blocking β1 subunit in DRG neurons (Ctrl, control; PTX, paclitaxel; Pue, puerarin). (A) Co-IP showed that paclitaxel treatment significantly increased the binding between Na_v1.8 and β1. n = 6 rats in each group. ^∗∗∗P < 0.001 compared with control group. (B,C) High resolution image showed that the colocalization between Na_v1.8 and β1 subunit in DRG neuron. n = 4 rats. ^∗∗∗P < 0.001 compared with control group. Scale bars: 5 μm (top) and 1 μm (bottom). (D) siRNA knock down the protein expression of β1 subunit in DRG. n = 6 rats in each group. ^∗∗∗P < 0.001 compared with scramble group. (E) Representative voltage-clamp recordings of Nav1.7 current in acute dissociated DRG neurons of day 10 paclitaxel-treated rats collected using a subtraction protocol (the current obtained following subtraction of the residual current following ProTx II administration from the total) the mean current density–voltage relationships are plotted in (D). n = 10 neurons in each group. (F,G) The IC₅₀ of puerarin on resting (F) or inactivated (G) state for Na_v1.8 in β1 subunit knock down and scramble DRG neurons of paclitaxel (day 10) rats. n = 10 neurons in each data point.