To evaluate the effect of mint leaf in reducing the neutrophil chemotaxis in lung tissue of Rattus norvegicus wistar. Methods: Twenty-eight Wistar rats were divided into four groups. In Group 1 (sham), only a laparotomy was performed. In Group 2 (positive control), the laparotomy was followed by upper mesenteric artery clamping and administration of beclomethasone via nebulization for ten minutes. In Group 3 (negative control) only the laparotomy and clamping were done. In Group 4 (mint), the laparotomy and clamping were followed by nebulization of mint leaf extract for ten minutes. All clamps were removed after forty-five minutes from their insertion and treatments, when performed, were instituted soon after. After ninety minutes of reperfusion, right lung base tissue samples were collected and properly stored from all rats. Results: In both Groups 2 and 4, there was reduction in inflammation in comparison to Group 3. Group 1 showed the lowest inflammatory cell count. Comparing average inflammatory cell counts of all groups to each other, there was statistical significance among all, except between groups 2 and 4. Conclusion: These results show that mint leaf extract is able to, trough nebulization treatment, significantly reduce the neutrophil chemotaxis in pulmonary tissue of Rattus norvegicus wistar subjected to induced acute lung injury.

γ-Aminobutyric acid (GABA) is the main inhibitory neurotransmitter in adult central nervous system (CNS) synapses, but it excites immature CNS neurons as well as neurons in the myenteric plexus. The present work aimed to determine whether GABA-induced nonadrenergic, noncholinergic (NANC) neuronal-mediated relaxation of the rat duodenum is dependent on the activity of Na+ K+ Cl- cotransporters (NKCC) and requires calcium influx. In the presence of guanethidine (3 µmol/L), atropine (3 µmol/L), and indomethacin (1 µmol/L), relaxations induced by GABA (100 µmol/L), KCl (5–10 mmol/L) and electrical field stimulation (1–8 Hz, 2 ms, 60 V), but not those induced by bradykinin (10–100 nmol/L) were abolished by lidocaine (300 µmol/L). However, only GABA-induced relaxations were reduced in a concentration-dependent manner by the NKCC1/2 inhibitors bumetanide (0.1–1 µmol/L) and furosemide (1–10 µmol/L). GABA-induced NANC neuronal relaxation was abolished by bicuculline (30 µmol/L) and inhibited by N-nitroarginine methyl ester (l-NAME, 300 µmol/L). The ω-conotoxin GVIA (1 µmol/L), which acts exclusively on neuronal CaV2 channels, but not on smooth muscle voltage-gated Ca2+ CaV1 channels, and nonselective blockers of these channels (verapamil 100 nmol/L and ruthenium red 10 µmol/L), reduced GABA-induced relaxations. These results showed that the activation of GABAA receptors induces NANC nitrergic neuronal relaxations in the rat duodenum, which depend on NKCC activity and CaV2 channel activation, suggesting that this phenomenon results from neuronal depolarization promoted by Cl− efflux through GABAA receptors, with subsequent Ca2+ influx and nitric oxide release.