Inflammatory cells apoptosis prevention

During chronic inflammatory disease, inflammatory cells (neutrophils, mast cells, macrophages, and lymphocytes) become increasingly more damaging to tissues. Anti-inflammatory action of Bik reduces cell death mediated by immune cell. Proinflammatory cytokine tumor necrosis factor-a (TNF-q) and interleukin-1 (3 (IL-1) cause expression of multiple inflammatory and innate immunity genes for additional cytokines, chemokines, adhesion molecules, and enzymes. Aprotinin has been reported to cause a reduction in apoptosis in vivo by decreasing inflammatory cytokine expression (IL-1, IL-6, and TNF -a) thus preventing caspase-8 activation [81],... 

Trigger programmed cell death (apoptosis) as opposed to random cell death (necrosis). This allows sub-lethal doses of photosensitiser, preventing damage and inflammatory response in healthy tissue. 

Insulin-dependent diabetes mellitus (IDDM) is an example of a metabolic disease under active consideration for inducible gene therapy strategies. In this disorder, inflammatory cytokines have been shown to activate apoptosis in pancreatic beta cells. Experimental studies indicate that expression of insulinlike growth factor-1 (IGF-1) can prevent the cytokine-mediated destruction of beta cells of the pancreas (Giannoukakis et al., 2001). Regulated expression of IGF-1 in human pancreatic islets, to preserve beta cell function, may be a useful approach in the treatment of certain types of diabetes (Demeterco and Levine, 2001). 

The biochemical mechanisms responsible for the cancer-preventive effects of green tea have not been clearly defined. Laboratory studies have shown that green tea possesses antioxidant and free radical scavenger activities, inhibits cell proliferation," induces apoptosis, modulates carcinogen-metabolizing enzymes, " - and suppresses inflammatory responses, - all of which could contribute to the observed preventive effects. 

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