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Nrf2 Pathway And The Reduction Of Oxidative Stress, Stephanie Jacobs Uselman
Nrf2 Pathway And The Reduction Of Oxidative Stress, Stephanie Jacobs Uselman
Physician Assistant Scholarly Project Posters
Oxidative stress has been linked to cellular damage initiating disease processes such as cardiovascular disease, diabetes, and cancer. The Nuclear factor erythroid-derived 2(Nrf2) pathway (Figure 1) aids in age-related cellular decline. The purpose of this study was to define the relationship between Protandim, its activation of the Nrf2 pathway, and decline in oxidative stress and cellular damage. The literature review included journal articles obtained from PubMed, Google scholar, and Cochrane review within the past 5-10 years, and contained both animal and human studies. The methods used in the animal studies included ANOVA, the standardized t-test, and the Neuman-Keuls post-test. P<0.05 was considered statistically significant. The human study included healthy participants, both male and female, age 29-78 with or without a specific medical diagnosis. Statistical analysis was based on the standardized t-test with a value of p<0.05 considered statistically significant. Liu et al. (2009) conducted a study investigating Protandim’s ability to suppress cancer tumor formation. Tumor incidence declined by 33% and multiplicity of skin tumors by 57% with p = 0.003. Superoxide dismutase increased 35%, catalase 58%, and manganese superoxide dismutase 21%. In 2013, Reuland et al. conducted a study to determine if Protandim could activate the Nrf2 pathway and induce antioxidant enzymes, thereby protecting cardiomyocytes from apoptosis. Results indicated that treated cardiomyocytes showed increased levels of Nrf2 nuclear accumulation, activation of endogenous antioxidant enzymes, and protection against cell targeted oxidative stress (p<0.05). Quereshi et al. (2010) completed a study to delineate if Protandim decreased oxidative stress through the Nrf2 pathway. After six months of supplementation, TBARS decreased by 48% (p=.006), and plasma osteopontin decreased by 57% (p=.018). In 2005, Nelson et al. conducted a study to determine if Protandim decreased cellular damage. After 30 days of supplementation, TBARS declined by 40% (p =0.0001), at 120 days, TBARS declined by 40-54% (p =0.002), and superoxide dismutase and catalase increased by 30% and 54% respectively. The results from studies indicate that Protandim’s activation of the Nrf2 pathway increased endogenous antioxidant availability, resulting in decreased oxidative stress and age related cellular damage.
Pcsk9 Inhibitors: A Review Of The Efficacy, Safety And Current Literature Recommendations, Lacey L. Jandrin
Pcsk9 Inhibitors: A Review Of The Efficacy, Safety And Current Literature Recommendations, Lacey L. Jandrin
Physician Assistant Scholarly Project Posters
Atherosclerotic cardiovascular disease is the leading cause of morbidity and mortality in developed counties. It is estimated that 60 million Americans have LDL-C levels > 160 mg/dl. Only about 1/3 of these patients meet treated LDL cholesterol goals of < 70 mg/dl indicating a need for greater control. High dose statins have been the mainstay in treatment of dyslipidemia, however, up to 20% of patients are statin intolerant indicating a need for secondary treatment strategies. This lead to the development of monoclonal antibodies to proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors. PCSK9 inhibitors result in decreased destruction of the low-density lipoprotein receptor (LDL-R) which leads to an increase in the transport of LDL-C to its destruction effectively reducing LDL-C levels in the blood. The purpose of this study is to analyze the literature available on the efficacy and safety of new PCSK9 inhibitors. The results of this literature review indicated that PCSK9 inhibitors effectively lowered LDL-C by an average of approximately 50%. The evidence reviewed by this analysis indicate that 70% of patients treated with PCSK9 inhibitors met LDL-C goals. The findings also indicate that the side effects associated with this new class of medications are comparable to current side effects seen with traditional cholesterol lowering agents. The largest side effect seen in up to 10% of patients were injection site reactions and did not require discontinuation of the medication. The results of this analysis indicate that PCSK9 inhibitors may be of benefit in patients who are statin intolerant, do not meet LDL-C goals on traditional statin therapy or have familial hypercholesterolemia. Education in use of injectables, cost and insurance coverage and dosing schedule are likely to be areas of continued research and may affect use of this new class of cholesterol lowering agents.