IntroductionAlteration in normal biochemical processes in a living tissue brought about by its response to both endogenous and exogenous stimuli, including physical stimulation such as change in temperature, pressure, pH, radiation, pathogens and chemical substances released by immune cells (inflammatory mediators) bradykinin, histamine, cytokines, hormones, change in available nutrients and abnormal partial pressure of oxygen (Gonzalez-Muniesa et al., 2015), as well as other environmental stresses, are one of the survival mechanisms of a living cell. However, inflammatory pathways play crucial roles in these biochemical processes. Inflammation defined as the body tissue response to injury (infection, trauma and hypersensitivity) is characterized in the acute phase by increase in the blood flow to the inflamed tissue caused by vasoactive-dependent vascular permeability mediators (nitric oxide (NO), prostacyclin, endothelin and endothelialderived hyperpolarizing factor) synthesized and released by endothelial cells leading to junctional opening and gap formation between endothelial cells which allows leakage of plasma and blood fluids (Galley & Webster, 2004). Moreover, while chemokines released by phagocytic cells recruit immune cells (leukocytes) to the inflammatory sites via increased expression of cellular adhesion molecules, their second important substances, cytokines (IL-1, IL-6, IL-8, IL-12, TNF-, NFkb) activate cellular immunity (Charles A Janeway, 2001). Nitric Oxide plays a pivotal role in the maintenance of cardiovascular homeostasis (Ritchie, Drummond, Sobey, De Silva, & Kemp-Harper, 2017). Its biosynthesis at high concentration by inducible nitric oxide synthase stimulates inflammation and induces apoptosis (Takasugi, 1993). Reactive oxygen species (ROS) mediates loss on NO bioavailability and functions via a non-enzymatic direct inactivation. Chronic inflammation is characterized by the development of specific humoral and cellular immune responses to the pathogens present at the site of tissue injury. These biochemical and cellular alterations are regulated by inflammatory mediators. In the last decade, intensive research into the mechanisms of inflammation has implicated several inflammatory triggering factors (infection, oxidative stress, PAMP, DAMP, radiation, thermal, chemicals, toxins, trauma/injury, hypersensitivity and immune response) and biochemical pathways (C-reactive protein synthesis, cyclooxygenase (COX) -1 and -2, lipoxygenase, nuclear factor kappa-B, tumor necrosis factor-α, adhesion molecules, nitric
