Open AccessMitochondrial KATP channels contribute to the protective effects of hydrogen sulfide against impairment of central chemoreception of rat offspring exposed to maternal cigarette smoke
Author(s) -
Lei Fang,
Wen Wang,
Yating Fu,
Wang Ji,
Yu Zheng
Publication year - 2020
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0237643
Subject(s) - offspring , apoptosis , mitochondrion , biology , medicine , potassium channel , endocrinology , pharmacology , microbiology and biotechnology , chemistry , biochemistry , genetics , pregnancy
We previously reported that maternal cigarette smoke (CS) exposure resulted in impairment of central chemoreception and induced mitochondrial dysfunction in offspring parafacial respiratory group (pFRG), the kernel for mammalian central chemoreception. We also found that hydrogen sulfide (H 2 S) could attenuate maternal CS exposure-induced impairment of central chemoreception in the rat offspring in vivo . Mitochondrial ATP sensitive potassium (mitoK ATP ) channel has been reported to play a significant role in mitochondrial functions and protect against apoptosis in neurons. Thus, we hypothesize here that mitoK ATP channel plays a role in the protective effects of H 2 S on neonatal central chemoreception in maternal CS-exposed rats. Our findings revealed that pretreatment with NaHS (donor of H 2 S, 22.4mM) reversed the central chemosensitivity decreased by maternal CS exposure, and also inhibited cell apoptosis in offspring pFRG, however, 5-HD (blocker of mitoK ATP channels, 19mM) attenuated the protective effects of NaHS. In addition, NaHS declined pro-apoptotic proteins related to mitochondrial pathway apoptosis in CS rat offspring pFRG, such as Bax, Cytochrome C, caspase9 and caspase3. NaHS or 5-HD alone had no significant effect on above indexes. These results suggest that mitoK ATP channels play an important role in the protective effect of H 2 S against impairment of central chemoreception via anti-apoptosis in pFRG of rat offspring exposed to maternal CS.