Pharmacological effects of basil: qualitative and quantitative studies

In this study, the pharmacological effects of purple basilicum (Ocimum basilicum var. purpurascens) extract (MFE; 40 µl/ml) in isolated mouse (Swiss albino, male, 25-30 g) bladder strips were investigated. In in vitro qualitative studies, the effects of MFE on contractile responses in isolated mouse bladder strips induced by electrical field stimulation (EAS; 5,10,20Hz; 1ms, 40V) of MFE and the molecular mechanisms involved in these effects (cholinergic system, nitrergic system, potassium channels and the roles of L-type calcium channels) were investigated. In in vitro quantitative studies, the anti-inflammatory and antioxidant effects of MFE in isolated mouse bladder were investigated. After opening the abdomen and isolating the bladders of mice euthanized by cervical dislocation under Ketamine/Xylazine anesthesia, in in vitro qualitative experiments, the bladders were divided into two equal parts through a longitudinal incision and stripped, and Krebs-Henseleit solution gassed with 5%CO2+95%O2 at 37oC 0.5 g of tonus was applied to a 10 ml organ bath containing. The answers were recorded in a computer-equipped pharmacological data analysis system (BIOPAC, MP35 Data Acquisition System) with an isometric transducer. In in vitro quantitative experiments, isolated mouse bladder tissues were homogenized after incubation (40 min) with MFE (40 µl/ml) and the effects of basil on cyclooxygenase (COX) and superoxide dismutase (SOD) in the supernatants obtained after centrifugation ELISA(Enzyme-LinkedImmunoSorbentAssay) analyzed by the method. In in vitro qualitative experiments, all of the isolated mouse bladder strip contractions induced by EAS were statistically significantly inhibited by MFE. In contrast, atropine, a nonselective antagonist of cholinergic muscarinic receptors, caused a statistically significant increase in EAS-induced contractions in the relevant tissues compared to control. In the combination of MFE + Atropine, it was observed that MFE inhibited the effect of atropine in a statistically significant way. Similarly, L-NOARG, an inhibitor of NO synthase, potentiated EAS contractions. In the combination of MFE+L-NOARG, it was observed that MFE inhibited the effect of L-NOARG in a statistically significant way. In addition, tetraethylammonium (TEA), a nonselective blocker of potassium channels, significantly increased EAS contractions compared to control. In the combination of TEA+MFE, it was observed that MFE inhibited the effect of TEA in a statistically significant way. On the other hand, verapamil, an L-type calcium channel blocker, caused a statistically significant decrease in contractile responses in EAS-induced isolated mouse bladder strips compared to the control. In the combination of verapamil + MFE, it was observed that MFE potentiated the inhibitory effect of verapamil. In in vitro quantitative studies, it was observed that MFE(40 µl/ml) decreased the cyclooxygenase (COX) enzyme level compared to the control group, but this decrease was not statistically significant. In experiments investigating the antioxidant effect of MFE, it was observed that although MFE caused an obvious increase in superoxide dismutase (SOD) enzyme levels, this increase was not statistically significant. As a result; in vitro qualitative experimental findings show that MFE has an inhibitory effect on contractile responses induced by EAS, and that cholinergic pathway, nitrergic pathway, potassium channel activation and calcium channel inhibition play a role in this inhibitory effect. In addition, experimental results suggest that MFE has no anti-inflammatory and antioxidant effects at the applied concentration.