Cyclooxygenase-1 and -2 (COX-1/2) catalyze the initial step in the formation of prostaglandins. Very recently their role in carcinogenesis has become more evident. They influence apoptosis, angiogenesis, and invasion, and play a key role in the production of carcinogens. Usually, a high level of COX-2 expression is found in cancer cells. Large epidemiological trials studying users and non-users of aspirin have shown that cyclooxygenase inhibitors and non-steroidal anti-inflammatory drugs (NSAIDs) could be of benefit against the development and growth of malignancies. Moreover, clinical trials in patients with familial adenomatosis polyposis syndrome have shown the efficacy of selective COX-2 inhibitors in the reduction of the number and size of colorectal polyps. Several preclinical studies show promising results with combinatorial treatments of either chemotherapy or radiotherapy with COX inhibitors. Preclinical studies with the simultaneous use of inhibitors of the epidermal growth factor receptor and COX-2 inhibitors have shown also promising results. Encouraging results from the first clinical trials combining chemotherapy with COX-2 inhibitors in patients with cancer in the advanced and neoadjuvant setting have recently been reported. Thus, it appears that targeting the COX-2 pathway is a promising strategy in the prevention and treatment of solid tumors.

Lymphocyte infiltration into the intestinal tract in inflammatory bowel disease (IBD) is mediated by interaction between α4 integrin and its specific ligands. Development of monoclonal antibodies against α4 integrin allowed targeting of lymphocyte trafficking into the intestine as a novel therapeutic intervention. Natalizumab, vedolizumab, alicaforsen AJM300, rhuMAb β7, CCX282-B, and PF-00547,659 are few of monoclonal antibodies that have shown high promise in trials with the potential for more attractive benefit:risk ratio than currently available therapies. In this review, an attempt is made to underline the therapeutic potential and the safety of anti-adhesion molecule treatment in IBD.

Current advances in understanding of the pathogenesis of inflammatory bowel disease have encouraged the development of many new therapies targeted at specific and non-specific mediators of the inflammatory bowel disease inflammatory pathway. Crohn's disease and ulcerative colitis, two common inflammatory bowel diseases likely result from interaction of multiple genetic and environmental risk and protective factors, deregulation of mucosal immunity in gut and breakdown of delicate balance of proinflammatory and anti-inflammatory cytokines. Immunobiologic agents targeted against TNF, leukocyte adhesion, Th1 polarization, T cell activation, nuclear factor-kappaB (NF-kappaB), and others are being assessed and will open exciting perspectives on development of therapies for inflammatory bowel disease.

Hepatoprotective activity of the methanol extract of Litsea glutinosa (MELG) was investigated by inducing hepatotoxicity with CCl 4 and paracetamol in rats. Increased levels of biochemical parameters like aspartate transaminase, alanine transaminase, bilirubin and alkaline phophatase in serum, along with reduced activity of catalase and super oxide dismutase in liver were induced by paracetamol and CCl 4 . Hepatic tissue architecture was also distorted by the hepatotoxins. Oral administration of MELG (100-200 mg/kg) offered a significant dose dependent protection against paracetamol and CCl 4 induced hepatotoxicity and restored the levels of the biochemical parameters to control levels. The hepatoprotective activity of MELG against paracetamol and CCl 4 was comparable with silymarin, which was used as reference standard. The results of this study indicate that MELG has potent hepatoprotective action against paracetamol and CCl 4 induced hepatic damage in rats.

No abstract