156 Yimam et al. factor-kappaB (NF-kB), and tumor necrosis factor-alpha (TNF-α) (Altavilla et al., 2009). Augmented numbers of animal models have been developed in order to study nociception and the action of various analgesic drugs in animals. Most of these tests have overlapping mechanisms of action in pain perception in response to irritants. All models share hyperalgesia consistent with the action of prostaglandins for lo- cal peripheral sensitization and centrally mediated nociception pathways (Ferreira, Lorenzetti, & Correa, 1978). However, it is not uncommon to find bradykinin, his- tamine, and serotonin, as well as many other vasoactive substances that are released in acute inflammatory responses. Intraplantar injection of carrageenan into rat hind paw produces inflammation characterized by increased edema and plasma pro- tein exudation with neutrophil extravasations and elevated metabolites of arachi- donic acid from cyclooxygenase (COX) and lipoxygenase pathways (Gamache, Povlishock, & Ellis, 1986). Research has also shown that carrageenan-induced in- flammation in rats is associated with distinct phases in the inflammatory process. The initial phase lasting for 30–60 min after carrageenan injection is dominated by the release of histamine, serotonin, and kinins and then mediated by prostaglandin and leukotrienes, which act relatively late in the development of inflammation re- sponse. NSAIDs are known to prevent hyperalgesia of inflammation by blocking the prostaglandin pathway (Flower, 1974). Intraplantar injection of formalin is a commonly used model for acute inflamma- tory pain, in which rodents display spontaneous nociceptive behaviors comprised of flinching or licking or biting of the affected paw in two distinct phases (Dubuisson and Dennis, 1977). The two separate phases possibly show presence of two different types of pain. These characteristic periods of intense paw licking can be observed for the first 5 min for the early phase with the late phase lasting from 20 to 40 min after the injection of formalin. It is suggested that the early phase pain is due to a direct effect of formalin on nociceptors and that proinflammatory prostaglandins do not play an important role during this phase. The late phase pain is believed to be as a result of inflammation (Dubuisson & Dennis, 1977). Acetic acid-induced visceral pain in mice has long been used for screening of nar- cotics and NSAIDs-like compounds for their antinociceptive effects. It is a nonspe- cific model, which involves local peritoneal receptors. The abdominal constrictions elicited by mice consist of contractions of the abdominal muscle that progress pos- teriorly and usually end with simultaneous flexor extension of both hind limbs with arching of the back. Upon intraperitoneal administration of the phlogistic agent be- havioral response lasts for 30 min (Collier, Dinneen, Johnson, & Schneider, 1968; Moore, Oluyomi, Babbedge, Wallace, & Hart, 1991; 2000). Bioflavonoids isolated from plants have been extensively reported as anti- inflammatory compounds. Nevertheless, scarce data are available for their analgesic usage. For instance, aqueous extract of Acacia karroo stem bark in carrageenan and writhing animal model (Adedapo, Sofidiya, Masika, & Afolayan, 2008), bu- tanolic fraction of dried leaves of Acacia pennata in writhing and formalin mouse model (Dongmo, Nguelefack, & Lacaille-Dubois, 2005), baicalin in carrageenan evoked thermal hyperplasia (Chou, Chang, Li, Wong, & Yang, 2003), myricitrin and gossypin in writhing mouse model (Meotti et al., 2006; Viswanathan, Samban- tham, Reddy, & Kameswaran, 1984), Oligomeric procyjanidin, rutin, hyperoside,