Fig. 5.
QX-314 induces a transient receptor potential vanilloid 1 (TRPV1)-dependent cytotoxicity. (A) The fraction of viable human (h)TRPV1-expressing cells and native human embryonic kidney 293 (HEK-293) cells lacking TRP channels after incubation with different concentrations of QX-314 and capsaicin (CAP) with or without the TRPV1 antagonist 4-(3-chloro-2-pyridinyl)-N-[4-(1,1-dimethylethyl)phenyl]-1-piperazinecarboxamide (BCTC) (10 μM). (B) The fraction of viable human transient receptor potential cation channel, subfamily A, member 1 (hTRPA1)-expressing cells after incubation with different concentrations of QX-314 and acrolein with or without the TRPA1 antagonist HC-030031 (50 μM). (C–E) Viable hTRPV1- (C, E) and hTRPA1-expressing cells (D) incubated with different concentrations of lidocaine with and without BCTC (10 μM) and HC-030031 (50 μM), respectively. In A through D, cells were incubated for 15 min with substances, and cell death was assessed by staining after 24 h. In E, cell death was assessed after 1 h. Cells negative for annexin V and propidium iodide were considered viable. Data are mean ± SD. Statistical differences were assessed by one-way ANOVA with Tukey post hoc testing. *P < 0.05, **P <0.01, ***P < 0.001. n.s. = not significant.

QX-314 induces a transient receptor potential vanilloid 1 (TRPV1)-dependent cytotoxicity. (A) The fraction of viable human (h)TRPV1-expressing cells and native human embryonic kidney 293 (HEK-293) cells lacking TRP channels after incubation with different concentrations of QX-314 and capsaicin (CAP) with or without the TRPV1 antagonist 4-(3-chloro-2-pyridinyl)-N-[4-(1,1-dimethylethyl)phenyl]-1-piperazinecarboxamide (BCTC) (10 μM). (B) The fraction of viable human transient receptor potential cation channel, subfamily A, member 1 (hTRPA1)-expressing cells after incubation with different concentrations of QX-314 and acrolein with or without the TRPA1 antagonist HC-030031 (50 μM). (CE) Viable hTRPV1- (C, E) and hTRPA1-expressing cells (D) incubated with different concentrations of lidocaine with and without BCTC (10 μM) and HC-030031 (50 μM), respectively. In A through D, cells were incubated for 15 min with substances, and cell death was assessed by staining after 24 h. In E, cell death was assessed after 1 h. Cells negative for annexin V and propidium iodide were considered viable. Data are mean ± SD. Statistical differences were assessed by one-way ANOVA with Tukey post hoc testing. *P < 0.05, **P <0.01, ***P < 0.001. n.s. = not significant.

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