The formalin test involves continuous pain generated by injured tissue, and
The formalin test involves continuous pain generated by injured tissue, and is PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/28914615 a very useful method, not only for assessing antinoci ceptive drugs, but also to help elucidate the mechanism of action. The neurogenic phase is probably a direct result of C-fibre activation due to the peripheral stimulus in the paw and reflects centrally mediated pain with the release of substance P. The late phase appears to be dependent on the combination of inflammation in the peripheral RG1662 site tissue with the release of histamine, serotonin,Lima et al. BMC Complementary and Alternative Medicine 2013, 13:195 http://www.biomedcentral.com/1472-6882/13/Page 5 ofFigure 1 HPLC-DAD chromatogram at 205 nm of the extract from Dioscorea villosa.bradykinin and prostaglandins [33-35]. Dioscorea villosa had analgesic effects in both the first and second phase of formalin-induced pain (p < 0.0001). In the first phase (Figure 3a) neurogenic-induced pain not was blocked at 100 (27.29 inhibition) or 200 mg/kg (p > 0.05) (30.06 inhibition), only the 400 mg/kg (46.06 inhibition) dose significantly blocked neurogenic pain. ASA (200 mg/kg; 52.2 inhibition) and MOR (98.76 inhibition) were significantly active in first phase (p < 0.05). This result shows the dose of 400 mg/kg is analgesic. In the second phase, representing inflammatory pain, DV significantly reduced licking time compared to the control group at 200 (51.36 inhibition) and 400 mg/kg (66.7 inhibition) (Figure 3b). Thus, higher doses of the extract were able to block both phases of the formalin response, but the effect was more prominent in the second phase. Together these results support the hypothesis that DV participates in the inhibition PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/27741243 of prostaglandin synthesis or the inhibition of proinflammatory cytokines (such asFigure 2 Effects of Dioscorea villosa (DV) on the acetic acid-induced writhing test in mice. Vehicle (control, per os or p.o.), morphine (MOR 3 mg/Kg, i.p) and DV (100, 200 and 400 mg/kg, per os or p.o.) were administered 1,0 hr before acetic acid injection. Each column represents mean ?S.E.M. (n = 6). ***p < 0.0001 versus control (ANOVA followed by Tukey’s test).Lima et al. BMC Complementary and Alternative Medicine 2013, 13:195 http://www.biomedcentral.com/1472-6882/13/Page 6 ofFigure 3 Effects of Dioscorea villosa (DV) on the formalin-induced nociception in mice (first phase ?Figure 2a and second phase Figure 2b). Vehicle (control) and DV (100, 200 and 400 mg/kg) were administered per os or p.o. 1,0 hr before formalin injection. The acetylsali-cylic acid (ASA) or morphine (MOR) were administered i.p. 0.5 hr before formalin injection. Each column represents mean ?S.E.M. (n = 6). **p < 0.001 or ***p < 0.0001 versus control (ANOVA followed by Tukey’s test).TNF-) and suggests the partial involvement of analgesic central pathways.Anti-inflammatory studieshave shown that diosgenin plays an important pharmacological role as an anti-inflammatory agent [43] by inhibiting the release of cytokines, such as TNF- [42].Toxicological studies Toxicity studyThe mechanism involved in the genesis of the carra geenan-induced oedema can cause the release of prostaglandins and kinins, as well as other substances such as prostaglandins, histamine, serotonin and leukotrienes. This type of oedema is dependent on the mobilisation of neutrophils [36-40]. The antiinflammatory effect of DV can be observed from its inhibitory action on carrageenan-induced leukocyte migration to the peritoneal cavity 4 h after stimulus wit.