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. 2023 Aug 6;30(2):e14379. doi: 10.1111/cns.14379

FIGURE 2.

FIGURE 2

Both BTN and NEM improved hypoxia‐induced [Cl−]i dysregulation and survival in neuronal cultures, and also preserved BDNF and GABAAR subunit balance. Primary hippocampal neuronal cultures were subjected to hypoxia followed by reoxygenation with or without PS‐low or BTN or NEM. (A) Flow cytometry on intracellular [Cl−]i concentration detected by MQAE and quantification. (B) Neuronal viability measured by CCK‐8. (C) Neuronal death measured by LDH release. (D) Western blotting and semi‐quantification of BDNF levels. (E) Western blotting and semi‐quantification of GABAAR α1 levels. (F) Western blotting and semi‐quantification of GABAAR α5 levels. MQAE: N‐(ethoxycarbonylmethyl)‐6‐methoxy‐quinoline bromide. BDNF, brain‐derived neurotrophic factor; BTN, bumetanide; CCK, cell counting kit; GABA, γ‐aminobutyric acid; LDH, lactic dehydrogenase; NEM, N‐ethylmaleimide; PS‐low, sub‐anesthetic dose of combined propofol and sevoflurane. Data are mean ± SD. *p < 0.05 versus control; # p < 0.05 versus hypoxia.