The Department of Pharmacology and Pathology,
Medical Faculty University of Zagreb, Zagreb, Croatia published this paper in 2010
“HIGH HEPATOTOXIC DOSE OF PARACETAMOL PRODUCES GENERALIZED
CONVULSIONS AND BRAIN DAMAGE IN RATS. A COUNTERACTION WITH
THE STABLE GASTRIC PENTADECAPEPTIDE BPC 157 (PL 14736)”
To demonstrate possible BPC 157 therapy capability as a paracetamol antidote in early and advanced stage of paracetamol toxicity, BPC 157 was applied intraperitoneally or intragastrically (12, 13) (i) prophylactically, immediately after paracetamol or (ii) therapeutically, after 3 hours elapsed.
Presenting the generally known significance of paracetamol toxicity (1-3, 6, 11), this may reveal the role of BPC 157 (i.e., a free radical scavenger (17, 29)) against the early paracetamol lesions development, and even more importantly, when the original damaging process induced by an extreme paracetamol over-dose was highly advanced.
“However, we shown that pentadecapeptide BPC 157, as an antiulcer peptide (12-15), may consistently counteract all paracetamol disturbances. This may also indicate that these disturbances are also interconnected throughout BPC 157 background. Moreover, considering the used paracetamol (5 g/kg i.p.)/BPC 157 (10 µg, 10 ng, 10 pg/kg i.p. or i.g., and effectiveness within µg-ng range) ratio (12, 13), it may be reasonably to assume that these therapy effects may indicate a likely role of BPC 157 in controlling, and then, counteracting one or more causative process(es).”
“What’s more, the premise that when given peripherally, BPC 157 may have a particular beneficial effect on CNS (i.e., markedly less damaged neurons in most severely injuried areas) is in accord with: its neuroprotective properties (22, 34), consistent antagonization of different central disturbances (16-23, 34),…”
“Also, BPC 157 was found to have anti-convulsive properties (16, 17, 21).
Also very recently, with the respect of K+-ATP channels in the substantia nigra as a predisposing factor for seizure development, BPC 157 inhibits K+ conductance in WT HEK293 cells (36).
Besides, after an induced traumatic brain injury in mice, BPC 157 regimens (corresponding to those used in the present study) demonstrated a marked attenuation of damage with an improved early outcome and a minimal postponed mortality throughout a 24 h post-injury period.
Ultimately, the traumatic lesions (subarachnoidal and intraventricular haemorrhage, brain laceration, haemorrhagic laceration) were less intense and consecutive brain edema had considerably improved (22).”
“In conclusion, we showed the progressive hepatic encephalopathy, accompanied by severe seizures with a very early onset, in paracetamol-rats (i.e., the full threatening circuit in paracetamol’s acute hepatic toxicity).
This was consistently counteracted by the stable gastric pentadecapeptide BPC 157, showing this peptide as an effective antidote therapy (i.e., given in µg- and ng-dose regimens in either stage of paracetamol intoxication).
Also, when given parenterally or per-orally (i.e., stable in human gastric juice for more than 24 h (12, 13)), in the same dose-regimens, BPC 157 protected against various agents or procedures that would otherwise have lead to severe liver lesions (29-31) or CNS disturbances (16-23).”
“Finally, BPC 157 counteracted a particular overdose toxicity that excided regular paracetamol regimens (i.e., 1, 2, 6, 11), at either of the assessed intervals (i.e., 25 min, 3 hours and 24 hours). On the other hand, the demonstration of paracetamol’s progressive hepatic encephalopathy with severe seizures at least partly overruled the general discordance of NSAIDs’ adverse effects and therapeutic application, paracetamol in particular as previously mentioned (1-10).
Also, the significance of this peptide’s therapeutic benefit against amplified and advanced paracetamol toxicity remains to be further postulated, particularly considering the extensive investigation of gastrointestinal peptides in gastrointestinal and liver physiology (38), physiological mediators in NSAIDs-induced impairment of gastric mucosal defense and adaptation (39), and brain-gut peptide regulation (40). However, very recent novel evidence suggested that just the stable gastric pentadecapeptide BPC 157 may have possible significance and implications for novel mediator of both Robert’s cytoprotection and adaptive cytoprotection (41), and thereby potential to counteract paracetamol and other NSAIDs (over)-toxicity.”
Source of the paper: http://www.jpp.krakow.pl/journal/archive/04_10/articles/15_article.html
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