A clarification for everyone who is interested in BPC-157

While I get the point of the post, as BPC-157 is not traditionally used as an antidepressant, there is some research out there showing it might have some benefits that are not necessarily related to its healing effects.

The antidepressant effect of an antiulcer pentadecapeptide BPC 157 in Porsolt’s test and chronic unpredictable stress in rats. A comparison with antidepressants

In these experiments, pentadecapeptide BPC 157, primarily designated as an antiulcer agent with cyto/organoprotective activity [21, 23, 25-30], was shown to reduce the duration of immobility in a way that might be typical of the re-uptake (serotonin, noradrenaline) of inhibitor antidepressants [38]. Of note, a positive effect was consistently observed in both of the tested models. In general, these findings were obtained in these two distinctive models, using the same doses of tested agents, pentadecapeptide BPC 157, and reference agents. Consequently, it seems likely that these salutary effects are not accidental. This may suggest a particular action, specially in the light of the previously mentioned recently described pentadecapeptide BPC 157 effects on variously disturbed animal behaviour [6].

Furthermore, as mentioned before, this pentadecapeptide, particularly interacting with the central dopamine system (i.e., in protection of gastric mucosa during stress) [27], also blocks the stereotypy produced acutely by amphetamine in rats. Likewise, this pentadecapeptide inhibits the development of haloperidol-induced supersensitivity to amphetamine in mice. Together, these data were interpreted as a particular modulatory activity of this pentadecapeptide rather than an interaction at receptor sites [6]. Theoretically, such an activity may be favourably used for the antidepressant activity.

It's a lot more complex than just healing of damage already caused. BPC-157 seems to possibly possess the ability to modulate various body systems, like dopamine, which may lead to acute antidepressant effects. I still would not promote its use as an antidepressant given the current research. However, I think there might be more to the story than just healing past damage. Take a look at he below study.

A novel pentadecapeptide, BPC 157, blocks the stereotypy produced acutely by amphetamine and the development of haloperidol-induced supersensitivity to amphetamine

In general, indirectly acting sympathomimetic drugs such as amphetamines have the common property of causing both increased calecholamine release and inhibition of catecholamine reuptake (primarily dopamine) at nerve endings in the central nervous system (e.g., Parkes 1974; Groves and Rebec 1976; Moore 1967). In this, stereotypic behavior appears to be the result of the activation of the dopaminergic system in the corpus striatum (e.g., Parkes 1974; Randrup and Munkvard 1966, 1967). There is evidence that pentadecapeptide BPC 157 is very effective when applied simultaneously with amphetamine in attenuating stereotypic behavior. This suggests an immediate interference with amphetamine activity. Interestingly, although increased stereotypic behavior may be an indication of already engendered amphetamine activity (e.g., Parkes 1974), this pentadecapeptide is still effective. On the contrary, even a lower dose of the pentadecapeptide (i.e., 10 ng/kg IP) appears to be effective in reducing stereotypic behavior. If applied at the maximum of amphetamine stereotypy, the smaller dose would reverse the otherwise prominent stereotypy as well. Given prophylactically, simultaneously with amphetamine, the ability to effectively counteract the amphetamine stereotypy appears to be limited to the higher dosage; the lower dosage would not reach the level of significance.

The inhibiting effect of pentadecapeptide on amphetamine-induced stereotypy appears to be rather specific. Namely, the increased excitability (a strong or violent twitching, panic jumping, and escaping) that appeared in control amphetamine-treated rats after a uniform sound challenge, was reduced by both high and low dosages. This occurred when pentadecapeptide was given either prophylactically as a cotreatment, or later, in an already highly advanced amphetamine disturbance, as a therapeutical medication. In comparison with the effect noted in antagonization of the amphetamine stereotypies, these disturbances could be counteracted with a relatively low pentadecapeptide dosage (particularly in the prophylactic regimen). Importantly, pentadecapeptide BPC 157 alone does not induce stereotypy, nor does it affect gross behavior (Sikiri6 et al 1993b).

Thus, taken together, these data suggest that this pentadecapeptide could have a modulatory effect on the dopamine system. In the condition of increased dopamine release and synthesis induced by amphetamine, it could both prevent and reverse the consequent disturbances (i.e., stereotypic behavior). Similarly, it could markedly attenuate the consequence of dopamine receptor blockade by haloperidol. This would suggest that this pentadecapeptide modulatory effect also implies, in some way, a substitution of the otherwise prominently insufficient dopamine system, avoiding the subsequent dopamine receptor supersensitivity and raised amphetamine disturbances. Thus, although the suggested special interaction with the dopamine system could be interesting from both theoretical and practical points of view.

So it seems that BPC-157 has a direct modulatory effect on the dopamine system, and can prevent/reverse disturbances from amphetamine use. Take a look at the other study below as well.

Central Serotonin Syndrome: Part II—Pathophysiology, Drug Interactions, and Treatment

An agent being considered for future treatment of serotonin syndrome is the gastric pentadecapeptide BPC 157. This peptide was initially investigated as a drug to control inflammatory bowel disease due to its interactions with serotonin in the gastrointestinal tract.44 Currently, there is indication that this peptide also has effects on central serotonin levels as well. Animal data suggest that BPC157, through suspected antagonistic effects at the 5HT2A receptor, can prevent symptoms of serotonin syndrome in rats given pargyline (irreversible monoamine oxidase inhi-bition)/L-tryptophan.44 Additional study is still needed before this agent can be recommended as a treatment.

So it seems that BPC-157 might also be a 5-HT2A antagonist, which can affect serotonin levels in the brain and possibly prevent serotonin syndrome.

Gastric pentadecapeptide BPC 157 effective against serotonin syndrome in rats

In all experiments, gastric pentadecapeptide BPC 157 contrasts with serotonin-syndrome either (i) presentation (i.e., particularly counteracted) or (ii) initiation (i.e., neither a serotonin substrate (counteraction of pargyline), nor an inductor for serotonin syndrome (no influence on l -tryptophan challenge)). Indicatively, severe serotonin syndrome in pargyline+ l -tryptophan rats is considerably inhibited even by lower pentadecapeptide BPC 157 doses regimens (particularly disturbances such as hyperthermia and wet dog shake thought to be related to stimulation of 5-HT 2A receptors), while the highest pentadecapeptide dose counteracts mild disturbances present in pargyline rats (mild hypothermia, feeble hind limbs abduction). Thereby, in severe serotonin syndrome, gastric pentadecapeptide BPC 157 (alone, no behavioral or temperature effect) has a beneficial activity, which is likely, particular, and mostly related to a rather specific counteraction of 5-HT 2A receptors phenomena.

So I think there is more to BPC-157 that we initially thought. In fact, I am glad this got brought up, because now I have a renewed interest in researching it. We brought out BPC-157 years ago, mostly for the healing properties. I used it to heal my shoulder after a couple failed surgeries, and it worked very well for that. I've been using it recently to heal some more injuries related to mountain biking. However, these dopamine and serotonin actions are making me more interested in other applications for it.