Yes it most certainly does.
Here's the discussion section from The Effect Of Pentadecapeptide Bpc 157 On Inflammatory, Non-Inflammatory, Direct And Indirect Pain And Capsaicin Neurotoxicity, P. Sikiri, Inflammopharmacology 1993, Volume 2, Issue 2, Pp 121-127
Note: Nociception (also nocioception or nociperception) is the encoding and processing of harmful stimuli in the nervous system, and, therefore, the ability of a body to sense potential harm.
DISCUSSION
The involvement of BPC in nociception as shown by these results, seems to be in line with the behaviour of a number of peptides known to be present in the different pathways subserving pain [17,18]. The possible analgesic mechanism of the peptide appears to be complex.
This seems to be supported by the evidence that BPC 157 reduced the nociceptive response in various assays, involving apparently different pathways, including both indirect as well as direct pain stimulation [6-17], such as that seen with acetic acid (liberation of one or more substances exciting nociceptors) and magnesium sulphate (direct stimulation of peritoneal nociceptors) [8-11]. The acetic acid assay, as a model of inflammatory, PG-dependent pain, has been connected both with acute inflammation of the peritoneal area [8] and with increased levels of PGE~. PGF~ [19,20] as well as malondialdehyde (MDA), a metabolite formed during PG~synthe~xs from endoperoxides in peritoneal fluid [9,10]. While the magnesium sulphate assay is considered to be a model of non-inflammatory and non-prostaglandin-dependent pain, since there are no changes in either PG release in the peritoneum, or in MDA concentration in the peritoneal fluid [9,10]. Consistent with those differences, the NSAIDs, serotonin and histamine-receptor-blocking drugs and morphine (known to be effective in acetic acid assay) are active only in much higher dosages, if at all, in the magnesium sulphate assay [9,10]. Interestingly, BPC 157 seems to be more effective in the magnesium sulphate than in the acetic acid assay. Hence, besides a modulation of the pain-producing effect of PGs and other substances, BPC 157 also appears to have an immediate (since it is effective when applied simultaneously with magnesium sulphate) direct effect on peritoneal pain endings, which is likely to be unrelated to PGs [8-111.
Consequently, it seems that the BPC 157 analgesic effect could be different from that of NSAIDs or morphine. This seems to be supported by the evidence that BPC 157 is more active than aspirin in, e.g. the tail pinching test. Likewise, in contrast to morphine, BPC 157 was not effective in the hot-plate test on naive mice or rats. Finally, the influence of BPC 157 on pain modulation, in line with its strong anti-inflammatory effect, should be viewed in conjunction with its proposed organoprotective effects [1-4], particularly a prominent gastrointestinal protection and a beneficial effect in wound healing and haemorrhagic shock (unlike the deleterious effect of NSAIDs or endogenous opioides [4,21-23].
The peptide's specific activity in nociception seems to be supported by its influence on allodynia in animals treated with a neurotoxic dose of capsaicin [17] and later subjected to the hot-plate test. Since, in this assay, BPC 157 had no influence on the normal pain reaction in naive animals, and, when given as a single pretreatment injection, it protected capsaicin-treated animals from neurotoxicity, a close interaction with eapsaicin seems likely. Furthermore, the development of capsaicin neurotoxicity was prevented by daily injection of BPC 157 while it had no influence after capsaicin degeneration had been established. Thus, it is possible that BPC 157 activity is related to the integrity of capsaicin-sensitive somatosensory neurons and their protection. Therefore, primary afferent neurons having small-diameter somata and unmyelinated (C-) or thinly myelinated (A/~-) fibres (as a main target of the sensory neuron-selective effects of capsaicin), and intracellular accumulation of calcium and NaC1, either slowly reversible or irreversible (with or without degeneration of neuronal soma), associated with quick defunctionalization and delayed depletion of cellular constituents and peptide transmitters (as final events implicated in the mechanism of the capsaicin neurotoxicity) [17], could be involved in BPC's action in nociception.
Those qualities, together with efficacy after oral application and no or negligible toxicity (100 mg/kg had no untoward effect in an acute toxicology study [4]), make BPC 157 an interesting tool for further research.
