Fig. 4: NRK-52E cells damage induced by H24R4 or/and LPS was regulated by the function of Cx43 channels. | Cell Death & Disease

Fig. 4: NRK-52E cells damage induced by H24R4 or/and LPS was regulated by the function of Cx43 channels.

From: Inhibition of gap junction composed of Cx43 prevents against acute kidney injury following liver transplantation

Fig. 4

a, b NRK-52E cells growth at low- and high-density cell culture exposed to H24R4, LPS (5 μg/ml, 24 h), or a combination of H24R4 and LPS. n = 6, *P < 0.05 vs control; #P < 0.05 vs the same treatment groups at low-density cell culture; △P < 0.05 vs the respective treatment of H24R4 or LPS. c, d Heptanol (2 mM, 1 h), Gap26 (300 μM, 1 h), and RA (10 μM, 24 h) had no effects on Cx43 expression in NRK-52E cells, but changed dye coupling. n = 5, *P < 0.05 vs control. The arrows were the donor cells. e Effects of heptanol (2 mM, 1 h), Gap26 (300 μM, 1 h), and RA (10 μM, 24 h) on cell growth at low- and high-density cell culture exposed to H24R4, LPS (5 μg/ml, 24 h), or a combination of H24R4 and LPS. n = 6, *P < 0.05 vs control; #P < 0.05 vs the same treatment groups at low-density cell culture. f Effects of heptanol (2 mM, 1 h), Gap26 (300 μM, 1 h), and RA (10 μM, 24 h) on LDH release at low- and high-density cell culture exposed to H24R4, LPS (5 μg/ml, 24 h), or a combination of H24R4 and LPS. n = 6, *P < 0.05 vs control; #P < 0.05 vs the same treatment groups at low-density cell culture

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