Abstract
The authors were not aware of errors made in one small subsection (Section 6.17. Antidiarrheal Effect, including the data in the table of effects) of this paper [1], and, hence, wish to make the following corrections to this paper. The authors wish to delete Section 6.17: Antidiarrheal Effect, including the data in the table of effects, and reorganize the references. The deleted section appears as follows: Diarrhea has long been a cause of death and illness in children and young animals [120,121,122]. Enterotoxigenic in ileus, E. coli (ETEC), and Vibrio cholerae are two primary microorganisms that cause diarrhea [123]. ETEC produces one or both of a heat-labile (LT) or heat-stable enterotoxin (either STa or STb), and V. cholerae releases cholera toxin (CT) [7]. Drugs, such as nicotinic acid, berberine sulfate, loperamide, and chlorpromazine, have been applied in animal models to inhibit the secretion of CT and LT [124,125,126]. Indomethacin, chlorpromazine, and berberine also decrease secretion induced by STa [124,126,127]. Despite the efficacy of these antisecretory compounds in animals, none are routinely available for use in humans because the doses required for efficacy are large enough to cause adverse side effects [128]. Over time, oral rehydration therapy was introduced, significantly improving patients’ mortality and morbidity with acute infectious diarrhea. Oral rehydration, however, does not hinder the secretion of toxins or alleviate diarrhea [129]. Scientists have demonstrated that bromelain has antidiarrheal properties [128,130]. A study by Mynott et al. (1997) used stem bromelain to demonstrate these antisecretory traits. The results showed that bromelain could prevent net changes in intestinal short-circuit current (Isc) using rabbit ileum installed in chambers, as well as mediate fluid secretion by secretagogues working via cAMP (cyclic-3′,5′-adenosine monophosphate), cGMP (cyclic-3′,5′-guanosine monophosphate), and calcium-dependent signaling pathways [131]. As one of these mechanisms is triggered by most toxins that induce diarrhea, bromelain is expected to be an important nutraceutical medication for this ailment. Bromelain was 62% effective in preventing LT-mediated secretion in this study, 51% effective against CT, and 35% effective against STa. Prostaglandin E2, theophylline, calcium-ionophore A23187, 8-Br-cAMP (8-bromo-cyclic-3′,5′-adenosine monophosphate), and 8-Br-cGMP (8-bromo-cyclic-3′,5′-guanosine monophosphate), well-known intracellular ion secretion mediators, also experienced secretory modifications. The effectiveness of bromelain has not been attributed to decreased tissue viability, due to its proteolytic effects on enterocytes, as shown by experiments measuring the absorption of nutrients into intestinal cells and others measuring the short-circuit response to glucose. A study performed by Roselli et al. (2007) on the impact of various plant extracts and natural substances (PENS) on ETEC-induced membrane damage in pig intestinal cells has shown that bromelain is among those with a protective effect [122].
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Chakraborty, A. J., Mitra, S., Tallei, T. E., Tareq, A. M., Nainu, F., Cicia, D., … Capasso, R. (2024, April 1). Correction to: Bromelain a Potential Bioactive Compound: A Comprehensive Overview from a Pharmacological Perspective (Life, (2021), 11, 4, (317), 10.3390/life11040317). Life. Multidisciplinary Digital Publishing Institute (MDPI). https://doi.org/10.3390/life14040483
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