Chronic inflammation is a pathological condition characterized by continued active inflammation response and tissue destruction. Many of the immune cells including macrophages, neutrophils and eosinophils are involved directly or by production of inflammatory cytokine production in pathology of chronic inflammation. From literatures, it is appear that there is a general concept that chronic inflammation can be a major cause of cancers and express aging processes. Moreover, many studies suggest that chronic inflammation could have serious role in wide variety of age-related diseases including diabetes, cardiovascular and autoimmune diseases. Inflammatory process induces oxidative stress and reduces cellular antioxidant capacity. Overproduced free radicals react with cell membrane fatty acids and proteins impairing their function permanently. In addition, free radicals can lead to mutation and DNA damage that can be a predisposing factor for cancer and age-related disorders. This article reviews the antioxidant defense systems, free radicals production and their role in cancer and age related diseases and also some of the recent patent relevant to the field. Study of the role of free radicals in human diseases can help the investigators to consider the antioxidants as proper agents in preventive medicine, especially for cancer and aging processes.

Recent epidemiological studies have demonstrated that metformin lowers the risk of several types of cancer in diabetic patients. Matrix metalloproteinases (MMPs) play a crucial role in the degradation of the vascular basement membrane extracellular matrix proteins, thereby promoting endothelial cell invasion, migration and angiogenesis in the incidence and progression of tumors. The aim of this study was to investigate the effects of metformin on human umbilical vein endothelial cell (HUVEC) proliferation and migration, as well as on MMP-2 and MMP-9 expression. Cell proliferation was determined by cell counting and MTT colorimetric assays. Cell migration was assessed by the wound repair method. Quantitative real-time reverse transcription PCR was performed to quantify the mRNA expression of MMPs. Metformin at concentrations of 0.5–3.0 mM effectively reduced the number of endothelial cells by 5.5–55%, without being cytotoxic to the cells. Similarly, cell proliferation and migration were markedly inhibited by metformin. In addition, treatment with metformin demonstrated a strong (P<0.001) suppressive effect on the mRNA levels of MMP-2 and -9 in the endothelial cells. The inhibitory effects of metformin on endothelial cell number, migration, and MMP expression were reversed partially by compound C, which is an inhibitor of AMP-activated protein kinase (AMPK). The present study reports that metformin considerably inhibited the proliferation, migration, and MMP-2 and -9 expression of HUVECs, and the effect was partially AMPK-dependent. The obtained findings provide a molecular rationale, whereby metformin can exert anticancer effects.

Corneal neovascularization (NV) is a significant complication of numerous infectious and non-infectious ocular surface disorders. Presence of newly formed blood vessels in the cornea can compromise clarity and therefore vision. Various growth factors and proteinases seem to be involved in the corneal NV. During corneal injury, angiogenic factors are released from corneal epithelial and stromal cells as well as infiltrating immune cells like macrophages. In fact, the balance between angiogenic and anti-angiogenic factors is shifted towards angiogenic molecules in the corneal NV. Numerous investigations support this idea that vascular endothelial growth factor (VEGF) plays a pivotal role in corneal NV by inducing endothelial cells proliferation, migration, and tubulogenesis. There is a growing body of evidence that corneal NV can be reduced by using anti-VEGF agents. This article reviews the most known molecular events in corneal NV and also some of the recent patents relevant to the field. Understanding the role of growth factors, proteinases and inflammatory cytokines in corneal NV can help the investigators to design therapeutic options for controlling this debilitating condition.

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