{'fraction_non_alphanumeric': 0.04862700228832952, 'fraction_numerical': 0.012585812356979404, 'mean_word_length': 6.080971659919029, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
The effect of nitric oxide donors on nitric oxide synthase‐expressing myenteric neurones in culture 1

Abstract  Previously, we demonstrated that intestinal inflammation leads to a postinflammatory loss of nitric oxide synthase (NOS)‐expressing myenteric neurones and motility disturbances. Here, we investigated whether high NO concentrations could be responsible for the decrease in NOS neurones. Myenteric neurone cultures, prepared from guinea‐pig small intestine, were incubated with NO donors [sodium nitroprusside (SNP) and 3‐morpholinosydnonimine (SIN‐1)]. After fixation, NOS neurones were identified by NADPH diaphorase staining and neurone‐specific enolase (NSE)‐positive neuronal content was assessed with an enzyme‐linked immunosorbent assay (ELISA)‐based method. Twenty‐four hours incubation with SIN‐1 (10−3 mol L−1) or SNP (10−4 mol L−1 or higher) reduced the number of NADPH diaphorase‐positive neurones. SNP incubation did not affect the NSE‐positive neuronal content. Shorter incubations (SNP: 4 and 12 h) had no significant effect. The SNP‐induced reduction was reversed by glutathione (GSH), but not by NO‐ or O‐scavengers, whereas GSH depletion enhanced the decrease. The NO‐dependent guanylate cyclase‐blocker 1H‐[1,2,4]oxadiazolo[4,3‐a]quinoxalin‐1‐one (ODQ) did not affect the SNP effect. This reduction can be explained by either specific apoptosis of NOS neurones or downregulation of NOS activity. However, TdT‐mediated X‐dUTP nick end labelling (TUNEL®) stainings argue in favour of the latter. In conclusion, the NO donor SNP decreases the number of NOS‐expressing myenteric neurones time and concentration dependently, without affecting the amount of neuronal material. Glutathione plays an important protective role.