proteins as well as altered matri protein synthe sis. This overall catabolic shift leads to changes in the tis sue structure that have been e tensively described in the literature. Although large structural changes can be observed during degeneration, this age related process does not necessarily cause pain symptoms. There is certain evidence in the literature that in a subgroup of patients, painful disc degeneration is characterized by increased levels of proinflammatory cytokines, e. g. interleukin 1B, interleukin 6, interleukin 8 and tumor necrosis factor. Although proinflammatory med iators seem to play a crucial role in intervertebral disc diseases, little is known about inflammatory pathways in intervertebral disc cells.

Results from studies on the pathogenesis of cartilage degeneration indicate that proinflammatory processes are mostly regulated by the transcription factor NF ��B, whose activity is tightly AV-951 regulated in vivo, e. g. by ac tivation of the so called Toll like receptors. Another important inflammatory pathway is the MAP kinase pathway that consists of a family of pro tein kinases with the major members being p38, ERK and JNK. Due to the lack of knowledge con cerning the molecular events underlying discogenic back pain, treatment of painful disc disease is cur rently limited, with typical options for the patient being conservative treatment and oral pain medication, both of which often only have a temporary effect. Other options are various types of surgical interventions, but these lead to high risks for the patients and high costs for the health care systems.

Therefore, research in the most recent past has concentrated on the development of minimal in vasive, yet effective new treatment options, covering approaches from cell and gene therapy to anti inflammatory substances for intradiscal injection. Currently, corticosteroidal substances are frequently used, which are known to have a significant risk for side effects and may cause disc space infections. Although research on biodrugs with regard to spinal diseases is yet rare, these novel anti inflammatory candidates could potentially benefit patients with dis cogenic back pain. Curcuma is a per ennial herb that is cultivated in Asian countries. As a powder, it has not only been used for cooking for centur ies, but also as a drug in the traditional Chinese and Indian medicine, treating e.

g. diabetic wounds, hepatic disorders, rheumatism and sinusitis. Numerous pub lications demonstrated an anti inflammatory effect of curcuma, with its effect probably being related to a class of substances called curcuminoids. Based on a thorough literature review, we hypothesize that curcuma has the potential to interfere with catabolic and inflammatory pathways. Hence, the aim of this study was to analyze the effects of curcuma e tracts as well as of one selected component of curcuma on IL 1B mediated cellular responses of human intervertebral disc cells in vitro. Additionally, its mechanism o