Ethanol gastric lesion aggravated by lung injury in rat. Therapy effect of antiulcer agents.
Stancic-Rokotov. D D; Sikiric. P P; Seiwerth. S S; Slobodnjak. Z Z; Aralica. J J; Aralica. G G; Perovic. D D; Anic. T T; Zoricic. I I; Buljat. G G; Prkacin. I I; Gjurasin. M M; Rucman. R R; Petek. M M; Turkovic. B B; Ivasovic. Z Z; Jagic. V V; Staresinic. M M; Boban-Blagaic. A A
Key Findings
- Lung injury makes ethanol‑induced gastric lesions more severe in rats
- BPC‑157 and other anti‑ulcer agents reduced gastric lesions even with prior lung damage
- Combined prophylactic and therapeutic dosing of BPC‑157 enhanced protection
Practical Outcomes
- BPC‑157 shows promise as a gut‑protective peptide, especially when taken before a known ulcer trigger and repeated later. However, because the data are from rats, any human use should start with very low doses and be approached cautiously, pending clinical evidence.
Summary
In rats, damaging the lungs first makes alcohol‑induced stomach ulcers worse, but giving anti‑ulcer drugs—including the peptide BPC‑157—protects the stomach. BPC‑157 worked whether given before or after the alcohol, and repeated dosing boosted its effect. This suggests BPC‑157 could help guard the gut against ulcer‑type damage, though it’s an animal study and human dosing isn’t known.
Abstract
Hemorrhagic mucosal lesions in the stomach in the rat induced by an intragastrical application of 1 ml of 50 or 75% ethanol were aggravated by preceding lung damage provoked by an intratracheal instillation of pyrogen-free saline or HCl (pH 1.75) or 50-h exposure to 100% oxygen. Due to the particular preceding aggravating circumstances, these lesions were taken to be of a special kind, rather than ordinary. So far, it is not known whether and how antiulcer agents may influence these lesions. Rats received an intratracheal (i.t.) HCl instillation [1.5 ml/kg HCl (pH 1.75)] (lung-lesion), and an intragastric instillation of 96% ethanol (gastric lesion; 1 ml/rat, 24 h after i.t. HCl instillation), and were sacrificed 1 h after ethanol. Basically, in lung injured rats, the subsequent ethanol-gastric lesion was markedly aggravated. This aggravation, however, in turn, did not affect the severity of the lung lesions in the further period, at least for a 1-h observation. Taking intratracheal HCl-instillation as time 0, a gastric pentadecapeptide, GEPPPGKPADDAGLV, M.W.1419, coded BPC 157 (PL-10, PLD-116; 10 microg, 10 ng, 10 pg), ranitidine (10 mg), atropine (10 mg), omeprazole (10 mg), were given [/kg, intraperitoneally (i.p.)] (1) once, only prophylactically [as a pre-treatment (at -1 h), or as a co-treatment (at 0)], or only therapeutically (at +18 h or +24 h); (2) repeatedly, combining prophylactic/therapeutic regimens [(-1 h)+(+24 h) or (0)+(+24 h)], or therapeutic/therapeutic regimens [(+18 h)+(+24 h)]. In general, the antiulcer agents did protect against ethanol gastric lesions regardless of the presence of the severe lung injury, in all of the used regimens. Of note, combining their prophylactic and salutary regimens (at -1 h/+24 h, or at 0/+24 h) may increase the antiulcer potential, and the effect that had been not seen already with single application, became prominent after repeated treatment.
Study Information
pubmed
2001
10.1016/s0928-4257(01)00040-7