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Laser photobiomodulation (LPBM) has been shown to be one of the possible modulating agents of inflammation. Similarly, medicinal plants, such as chamomile (Matricaria recutita) are also used with the same purpose. To evaluate tissue repair in the dorsum of the tongue of rats under topical use of chamomile alone and in association with LPBM. Seventy‐five male Wistar rats received a standardized wound on the dorsum of the tongue and were allocated into experimental groups: Control (G1), Chamomile Fluid extract (G2), Chamomile Infusion (G3), Laser (G4), Chamomile Infusion + Laser (G5). Euthanasia was done on days 3, 7, and 14 after surgery. Ulcers were evaluated and measured with a caliper. Sections stained with hematoxylin and eosin and Picrosirius Red allowed evaluation of edema, inflammatory infiltrate, cellularity, and re‐epithelialization and characterization of total collagen. Histomorphometric analysis of the percentage of total collagen, the distance from the basal layer to the epithelial surface, and the thickness of the stratum corneum were performed. The G2 and G4 groups modulated the exudative and proliferative phases of inflammation, both clinically and histologically. The G3 and G5 groups did not show significant differences in relation to the G1 group in most of the evaluated parameters. Chamomile fluid extract and LPBM alone showed better clinical and histological responses for tissue repair than the association between these therapeutic modalities. There were differences in the parameters of clinical, histological, and histomorphometric patterns between the experimental groups of the present investigation. The LPBM proved to be superior in the performed analysis. [ABSTRACT FROM AUTHOR]

Ayahuasca (AYA) is a psychedelic brew used in religious ceremonies. It is broadly used as a sacred medicine for treating several ailments, including pain of various origins. To investigate the antinociceptive effects of AYA and its mechanisms in preclinical models of acute and chronic pain in mice, in particular during experimental neuropathy. The antinociceptive effects of AYA administered orally were assessed in the following models of pain: formalin test, Complete Freund's Adjuvant (CFA)-induced inflammation, tail flick test, and partial sciatic nerve ligation model of neuropathic pain. Antagonism assays and Fos immunohistochemistry in the brain were performed. AYA-induced toxicity was investigated. AYA was chemically characterized. The antinociceptive effect of harmine, the major component present in AYA, was investigated. AYA (24–3000 μL/kg) dose-dependently reduced formalin-induced pain-like behaviors and CFA-induced mechanical allodynia but did not affect CFA-induced paw edema or tail flick latency. During experimental neuropathy, single treatments with AYA (24–3000 μL/kg) reduced mechanical allodynia; daily treatments once or twice a day for 14 days promoted consistent and sustained antinociception. The antinociceptive effect of AYA (600 μL/kg) was reverted by bicuculline (1 mg/kg) and methysergide (5 mg/kg), but not by naloxone (5 mg/kg), phaclofen (2 mg/kg), and rimonabant (10 mg/kg), suggesting the roles of GABA A and serotonergic receptors. AYA increased Fos expression in the ventrolateral periaqueductal gray and nucleus raphe magnus after 1 h, but not after 6 h or 14 days of daily treatments. AYA (600 μL/kg) twice a day for 14 days did not alter mice's motor function, spontaneous locomotion, body weight, food and water intake, hematological, biochemical, and histopathological parameters. Harmine (3.5 mg/kg) promoted consistent antinociception during experimental neuropathy. AYA promotes consistent antinociceptive effects in different mouse models of pain without inducing detectable toxic effects. Harmine is at least partially accountable for the antinociceptive properties of AYA. [Display omitted] [ABSTRACT FROM AUTHOR]