Propionate and Expression of NRF2 - Essay Example

Propionate and expression of NRF2 al Affiliation) Expression of NRF2 The expression of the transcriptionfactor. The basic zipper protein that regulates the expression of the antioxidation protein that care for the damages that are brought by the oxidative factors (Auf, 2005). The damages that are protected against by the factor are that occur due to injury and also inflammation. The drugs that are used in the treatment in the factor are those that cause by the oxidative stress. There is need in the neutralization of phase2 enzymes in the body. The neutralization is that that is to act indirectly to the antioxidant. This is done through the transicsicion factor of the Nrf2 enzymes. The enzyme combines it the antioxidant in the response elements. The enzyme is found in the upstream regulatory region of the respiratory surface and are linked to the genes that induce the actions of the enzymes (Leung, 2008). The cells ant the nuclear of the Nrf2 levels increase very fast and are persistent after the putting into treatment D3T but in the same time they are able to be blocked with cyclohemidate. Overexpression of the Nrf2 enzyme leads to the activity of the promoter of the enzyme making the expression of the enzyme mutant represses the activity. The enzyme can be thought to regulate own expression through the activities ARE- elements which are located in the proximal areas of its own promoter. Through the activities it leads to the accumulation of the enzyme and the protected inductions that come from it in the genes in the response to the chemo preventive agents. The expression of the NRF2 is kept in the cytoplasm by the proteins in the cells that decreases its value quickly. This is the condition that occur in the cells under the normal circumstances. There are target by the genes in the activation of the Nrf2. NAD is a prototypical target gene that is involve in the reduction and the detoxification and the highly reactive factors that brings about redox cycling and the oxidation stresses (Auf, 2005). Glutamate-cysteine ligase and glutamate-cysteine catalytic modifier are the characteristics that are targeted by the Nrf2 genes that are established by the regulator of glutathione. This is one of the most important antioxidant in the body due to the living cells and tissues. Thioredoxin reductase 1 and sulfiredoxin 1 are also the genes that are targeted by the factor. The genes are the ones that are involved in the reduction and the recovery of peroxiredoxins. The genes are also important in the detoxification of the highly reactive peroxides in the body in the inclusion of hydrogen peroxide. Heme oxygenase 1 is also a target gene. The enzyme catalysis the breaking down of antioxidant and also the anti-inflammatory such as carbon monoxide and protect from a varied range of pathologies. The protection is done also to the acute injuries that can affect the lungs, kidney injuries and also pain. Cytocolic, mitochondrial and also the microsomal enzymes and also the enzymes that are targeted by the factor (Leung, 2008). The factor leads to the detoxification and the elimination of toxic substances in the conjunction and coordination of other factors. The places that are occupied by Nrf2 are the essential parts of the body including, muscles, lungs, kidneys, the heart and the brain. There have been potential adverse effects that have been caused by the Nrf2 activation (Auf, 2005). The activation may cause the development of cancerous tumors and also resulting in the cholesterol level in the body majorly in the liver that in turn leads to the development of atherosclerosis. The continuous effects that are caused by the activation may be overshadowed by the benefits and the profits that might have led to the activation. There have been propionate effect on the factor Nrf2. The carbocysteine and fluticasone propionate that has occurred in the occurrence due to the use of factors such as cigar ate smoking that stimulates the bronchial epithelial cells. Smoking of cigarettes induce oxidative stress. The oxidation stress that comes about is an important feature in the pulmonary disease. The oxidative stress that is caused by the effect bring about poor clinical efficacy in the patient that suffer the effect (Leung, 2008). The effect that is brought by the carbocysteine is in the sense that it induces the oxidative stress in bronchial epithelial cells and also in the comparison of antioxidant effect and the fluticasone propionate being unknown. The effect on the survival of the cells and intercellular reactive oxygen species and also glutathione leads to the stimulation of the bronchial epithelial cells. Carbocysteine does not induce cell necrosis with in turn result in the increase in the ROS. Fluticasone in the fact does not modify the intercellular ROS production but results in the reduction in Nrsf2 that is stimulated. It differs with the carbocysteine which reduces the ROS production and nuclear expression that makes it more efficient in the modulation of effects. The use of carbocysteine is considered to be promising strategy that can be used in diseases that are associated with the resistance that occur in corticosteroid. Nrf2 has been signaled in the pathways as the most important cell that is needed and used in the survival. The factor protect cells and tissues from a variety of the factors that can lead to the toxification of the tissues and this is through the function that they do in the consideration of the several cytoprotective genes. The protection of Nrf2 is done to the normal cells and also in the cancer cells through the chemo preventive compound used in the clinical trials. The factor facilitate cancer regration in the body. Nrf2 is accumulated and associated in the prognosis in patients. Nrf2 is induced during the administering of drugs for resistance and contributes to both the basic and acquired chemo resistance. The acquired and the basic bring the understanding the role of Nrf2 in the treatment of cancer and the cancer cells. Curcumin through Nrf2 can be used in the inhibition of breast cancer but the inhibitor still remains unclear as the research is still on. The cancer is due to the DNA specific nuclear that contribute to the development. The regulation comes as the factor is a master regulation in the cellular antioxidant and defense systems. When the Nrf2 induces the translocation from the cytoplasm to the nucleus decreasing the promoter activities through the decreasing of the recruitment. The consumption of cancer cells is large in terms of nutrients and also in the maintenance of high level of anabolism.nrf2 brings about oncogenic pathways that are involved in the modulation of the metabolic reactions (Yates, 2009). The factor have been in the homeostatic functions of the body and have shown positive contribution to malignant phenotypes in cancer including those that comes with aggression proliferation. Nrf2 acceleration on the proliferation are not well understood. The nuclear accumulation of the factor accelerates the metabolic activities that come also with the cell prolification in the addition to enhance cytoprotection. The functional activities that expand Nrf2 reinforcement in the metabolic programming brought about by the proliferative signs. In the relationship between Nrf2 and the activation, the activation of the factor results in the increase in the uptake of glucose that takes place in the cells of the body. After the activation of the glucose, it is preferentially metabolized through the factors of PPP. The increase ion the levels is that it is not the only for the functional detoxification of the cells but it also depend on the gene expression in the cells of the mammals. The activation in the cells through the action makes it one of the major defenses that are against the xenobiotic stress. The activation influences the gene involvement in the metabolism of the genes. The metabolic responses that are brought together by Nrf2 in the separate nonmalignant cells of the body. Small molecule sulforaphane and the knockout of and the inhibitor of the factor leads to the increase addiction of fibroblast is for the glucose. The glucose is metabolized through the pentose phosphates that comes about after the activation with the increased production of NADPH generation (Yates, 2009). The protein in the unstressed conditions are kept in the lowest level possible through the binding of the most prominent ketch like inhibitor. There are several changes that occur when the protein is exposed to the oxidation state (Yates, 2009). In the exposure for the oxidation, keep 1 is the element that acts as the redox sensor and this is through the modification of some residues that comes out in the redox reaction for the oxidation. The interruption of the protein eliminates degradation and favors the coming to stable Nrf2 and continuous translocation to its nucleus. Nrf2 heterodimerises with proteins and binds them to elements in the promoters of the genes. The ones that are involved in the stage are the ones that undergoes drug metabolism, oxidases stress and the detoxification. The products that are attained from plants and animals are able to trigger the activation of Nrf2. This has made the protein a main focus in the explore as the main target for drugs and the supplements that are done to nutrition. The beneficial part of the protein leads to the coming up of some diseases in a body of a person. The diseases that ae brought about by the activation includes diabetes, vascular diseases and cancer (Harvey, 2011). The disorders that occur are those that occur due to the miss in the balance of redox in the balance to oxidative stress. The protein Nrf2 does not only perform the work of detoxification and antioxidation but it also plays an important role in the regulation of the clusters of the genes that are involved in the metabolism of glucose. The protein showed both benefits and also fail in the lipids depending on the system that is used in the administration. Making the cancer cells to cause the activation of the proteins. The metabolic adaptation of the protein can be ruled out through the treatment with the activator sulphorafane which proves it due to the lack of response in the isogenic cells. The adaptations are used to distinct rates of plorification upon the different treatments that are done to it. The loss of the protein Nrf2 bring about the depolarization of the mitochondria leading to impairment in the respiratory functions due to the decreased ATP levels. The activations leads to the efficiency in the oxidative. The protein cells have definitely increased the manufacturing of ATP through the process of glycolysis using a phase for the keeping of the maintenance of the potential of the membrane of the mitochondrion. Inhibition of respiration is slow when there is generation of the NAHD in the knockout cells as compared to other body cells (Harvey, 2011). The results shows that the Nrf2 directly is involved in the regulation of cellular metabolic activities in the body through the modulation of the availability of substrates for the activities of respiration of the mitochondria. The impact of the catalyze overexpression are related to the Nrf2 stimulation of the angiotensinogen gene that leads in the development of hypertension and the renal injury in the diabetes mice (Yates, 2009). The overexpression bring about the normalizing of systolic BP and inhibit the Nrf2 AGT. The enzyme is stimulated by the high glucose level, hydrogen peroxide and also in the vitro. The stimulation through the causes can be blocked by the trigonelline and the interference in the RNA and the enzymes and also the pharmacological inhibitors of the nuclear factor of the enzymes. Pollutants have caused proinflamatory effects to the body including the redox recycling the chemicals and the oxidative stress that occurs in the respiratory track. The antioxidant defense pathways have been done through the expression of the phase 2 enzymes. There is demonstration that the aromatic and the polar fractions which brings the expression of the phase 2 enzymes (Leung, 2008). The expression is mediated through the accumulation of the transcription factor. The enzymes in the nucleus targets the sites and this leads to the weakening of the response. From analysis it has been shown that there is increase in the expression of the pulmonary effects through the way that they bring the inflammation and also in the acting as the adjuvant for the production of other factors in the immunes system. The actions that occur in this way brings about the increased actions of the prevalence of asthma (Harvey, 2011). There however have been contradictions in the physical and also the chemical factors that determine the health risk of an individual. The ROS that is produced in this case have made them exceed the cell ability in the neutralization of the oxygen at the time when there is oxygen stress. The inactivation also is possible in the case. The stress in the activation brings about a number of redox sensitive signaling pathways that includes several cascades. The enzyme plays an active role in the expression of the proinfammatory cytokines and adhesion molecules. In the event of the signaling requires the PM doses that does the intermediate between the toxic and the protective amounts in the body. The actions have led to the development of oxidation stress that occurs in order in which the increase in the PM induce the effect of the protective and the dangerous effects to the body. The enzymes induces the cytoprotective, antioxidant and also the anti-inflammatory effects in the lungs of an individual. Sometimes there can be failure in the protection and when this occurs, escalation of the oxidative stress leads to the activation (Harvey, 2011). When the oxidative stress reaches the peak, perturbation of the mitochondrial permeability and the electron transfers in the body leads to the apoptosis and also necrosis in the cells. There has been understanding through this factors and mechanisms, the lung defenses against the pro oxidation and pro inflammation effects on the particular pollutants that leads to the causing of asthma. This can help in the characterization of those that are more prone to the development of asthma due to the defects that occur in the expression of the phase 2 enzymes. Propionate development Fluticasone propionate id based on the nucleus and is selected from the activity of the structure relationships which includes those of inflammatory, hypothalamic and cutaneous. The FP is a glucocorticoid based on the androstane nucleus. FP has high selectivity in the doing in the glucocortid receptor which occurs with the little or lack of an activity that links it to the steroid receptors. In asthma patients, it results to the reduction of cells in the bronchial biopsies (Leung, 2008). FP is linked also with the sexual development it induces characters in males that are together with absence of nipples and the absence of the tissues that makes one to be male like. It also brings the environmental androgens and the factors that are associated to the sexes in the individuals. The concentration of the factor leads to the masculine in the female and also leads to the altering of the male offspring. References Auf dem Keller, U. (2005). In vitro and in vivo function of Nrf2 in keratinocytes. Zürich. Harvey, C. (2011). Identification of an immunomodulatory role of Nrf2 in COPD exacerbations. Leung, L. (2008). Functional analyses of Nrf1 and Nrf2 transcription factors. Yates, M. (2009). Targeting Nrf2 signaling for cancer chemoprevention using synthetic triterpenoids. Read More