Adding exercise to rosuvastatin treatment: influence on C-reactive protein, monocyte toll-like receptor 4 expression, and inflammatory monocyte (CD14+CD16+) population

Coen, Paul M.; Flynn, Michael G.; Markofski, Melissa M.; Pence, Brandt D.; Hannemann, Robert E.

doi:10.1016/j.metabol.2010.05.002

Cited by 38 publications

(33 citation statements)

References 41 publications

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“…Имеются единичные исследования о влиянии ста-тинов на субпопуляционный состав моноцитов, и их результаты неоднозначны. Согласно одним исследо-ваниям [13], статины уменьшают количество цирку-лирующих неклассических моноцитов, согласно дру-гим [14], статины не оказывают существенного влия-ния на субпопуляции моноцитов. В ряде работ описано ингибирование статинами синтеза прово-спалительных цитокинов моноцитами.…”

Section: Discussionunclassified

The Influence of Atorvastatin and Rosuvastatin in Atherosclerosis on the Parameters of Cellular Immunity and in Vitro Leucocyte Activation

et al. 2018

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Цель. Провести сравнительный анализ влияния "липофильного" аторваста-тина и "гидрофильного" розувастатина на показатели клеточного иммунитета у пациентов с атеросклерозом. Материал и методы. В исследование было включено 35 пациентов в возрас-те 62 [57;68] лет, 18 мужчин и 17 женщин, направленных на обследование в ИКК им. А. Л. Мясникова с предварительным диагнозом ишемическая болезнь серд ца, атеросклероз коронарных и сонных артерий, и имеющих показания к интенсификации терапии статинами. У 17 пациентов доза ато-рвастатина была увеличена с 20 мг до 80 мг, у 18 пациентов -доза розува-статина с 10 мг до 40 мг. Всем пациентам исходно и через один месяц мето-дами прямой иммунофлуоресценции и проточной цитофлуориметрии прово-дилось определение содержания в периферической крови популяций лимфоцитов, включая регуляторные и эффекторные субпопуляции, и основ-ных фракций моноцитов. В условиях клеточной культуры изучено влияние аторвастатина и розувастатина на пролиферацию CD4+ Т-лимфоцитов и липополисахарид-индуцированный синтез цитокинов моноцитами, выде-ленных из крови доноров. Результаты. На фоне приема аторвастатина отмечено увеличение относи-тельного содержания циркулирующих регуляторных Т-лимфоцитов (Treg), увеличение соотношения Treg/Т-хелперы 17 (Th17) и уменьшение соотноше-ния активированные CD4+Т-клетки/Treg. Терапия розувастатином не сопровож-далась изменениями показателей клеточного иммунитета. Статины не вли -яли на субпопуляционный состав моноцитов крови. Обнаружено дозозависи-мое ингибирование статинами пролиферации CD4+ Т-лимфоцитов; действие аторвастатина проявлялось при концентрации 10 нмоль/л, розувастатина -в 10 раз выше. Введение статинов, 10-100 нмоль/л, в культуру моноцитов не влияло ни на спонтанную, ни на индуцированную эндотоксином секрецию цитокинов. Заключение. В терапевтических дозах аторвастатин обладает иммуномоду-лирующей активностью, проявляющейся в увеличении относительного содер-жания регуляторных субпопуляций Т-лимфоцитов крови, что может быть обусловлено подавлением пролиферации эффекторных клеток. THE INFLUENCE OF ATORVASTATIN AND ROSUVASTATIN IN ATHEROSCLEROSIS ON THE PARAMETERS OF CELLULAR IMMUNITY AND IN VITRO LEUCOCYTE ACTIVATIONFilatova A. Yu., Potekhina A. V., Ruleva N. Yu., Radyukhina N. V., Arefieva T. I. Aim.To compare the influence of "lipophilic" atorvastatin and "hydrophilic" rosuvastatin on the parameters of cellular immunity in atherosclerosis patients. Material and methods. Totally, 35 participants included, mean age 62 [57;68] y. o., 18 males and 17 females, directed for follow-up to Myasnikov Cardiovascular Center with preliminary diagnosis coronary heart disease, atherosclerosis of coronary and carotid arteries, and with indications for intensified statin therapy. In 17 patients the dosage of atorvastatin was increased from 20 to 80 mg, in 18 -dosage of rosuvastatin from 10 to 40 mg. All patients at baseline and in 1 month, by the methods of direct immune fluorescence and cytofluometry underwent the measurement of content of monocytes and lymphocyte populations in ...

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Section: Discussionunclassified

The Influence of Atorvastatin and Rosuvastatin in Atherosclerosis on the Parameters of Cellular Immunity and in Vitro Leucocyte Activation

et al. 2018

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“…It was associated with increases of DHEA and IGF-1 levels (Gonzalo-Calvo et al, 2011). Another study shows also that exercise reduces inflammatory monocytes in hypercholesterolemic patients (Coen et al, 2010). …”

Section: How Living Habits and Nutrition Status Impact On Immune Funcmentioning

confidence: 94%

“…Fenofibrate and simvastatine in type 2 diabetic patients with mixed dyslipidemia and in patients with hypercholesterolemia or impaired fasting glucose, reduce expression of TNF, IL-, IL-6 and MCP-1 by LPSstimulated monocytes. Both treatments significantly reduce high-sensitivity CRP levels (Krysiak et al, 2011b;Krysiak et al, 2011a) but there are conflicting results (Coen et al, 2010). Statin and aspirin decrease serum levels of IL-1 and C-reactive protein in hypercholesterolemic patients (Ferroni et al, 2003).…”

Section: Cardiovascular Diseases and Associated Metabolic Disordermentioning

confidence: 99%

Innate Immune Responses in the Geriatric Population

Compté¹,

Goriely²

2012

Recent Advances in Immunology to Target Cancer, Inflammation and Infections

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“…In addition, physical exercise may also prohibit promotion and progression stages of carcinogenesis by scavenging reactive oxygen species (ROS) [100]; altering cell proliferation, apoptosis, and differentiation [71]; decreasing inflammation [101]; and enhancing immune function and suppressing angiogenesis [99]. With this complex information, we will sum up previous reports and discuss potential mechanisms behind the relationship between PA and breast cancer in several aspects, from whole body and the metabolic system to molecular pathways [102][103][104][105] (Figure 1). …”

Section: Potential Mechanisms Behind Physical Exercise For Preventingmentioning

confidence: 99%

Potential Mechanisms behind Physical Exercise vs. Epigenetic Regulation for Preventing Breast Cancer

Dai¹,

Yang²,

Shi³

et al. 2017

JCPCR

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Potential Mechanisms behind Physical Exercise vs. Epigenetic Regulation for Preventing Breast CancerSubmit Manuscript | http://medcraveonline.com recent years, new applications in both diagnosis and treatment have gradually reduced female breast cancer incidence rates [1]. Considering alternative prevention and therapeutic methods, physical exercise has recently been gaining increased attention in the clinic. Regular exercise appears to lower breast cancer risk by about 10-20 percent, which is a considerable impact from a non-pharmacologic intervention with no cost. Thus, the recently emerging field of exercise-oncology research will be expected to not only clarify the mechanisms behind prevention, but also shed light on future treatment for breast cancer. In this current review, we will summarize recent studies on physical exercise with respect to breast cancer, and discuss their relationship and possible underlying mechanisms. Risk factors for breast cancerBreast cancer is the second most common type of cancer and the leading cause of cancer-related death in women worldwide (link: https://www.breastfriends.org). It is a tremendous disease, affecting lifespan and healthspan. The incidence of breast cancer is increasing every year, and an estimated 252,710 new cases of invasive breast cancer are expected to be diagnosed in women in the U.S. in 2017 (link: http://www.breastcancer.org/symptoms/ understand_bc/statistics). Throughout the world, every year more than 400,000 deaths are caused by breast cancer and, out of these diagnosed cases, there are more than 2.8 million breast cancer survivors [2].Generally, there are two aspects of risk factors for breast cancer (see Table1): (1) [68][69][70]. On the other hand, due to genetic susceptibility influences, which are inherited and unchangeable; the non-modifiable factors are not easily controllable risks for breast cancer. Therefore, it is feasible to reduce the risk factors that are not inherited, but can be changed. Among these modifiable risk factors, physical exercise behaviors not only are beneficial for preventing all stages of cancer development [71], but also are helpful to maintain a healthy weight and reduce risks for developing other diseases, such as cardiovascular disease, diabetes, and stroke [72]. Furthermore, physical activity (PA) has been increasingly regarded as the nonpharmacologic intervention for many cancer patients to combat both the physiologic and psychological effects of cancer treatment [73]. A recent World Health Organization (WHO) report shows that physical inactivity remains one of the most important risk factors for total cancer related mortality (responsible for 6% of total deaths) along with overweight and obesity (responsible for another 5%) [74]. AbstractBreast cancer is the most commonly diagnosed cancer and has been the second leading cause of death due to cancer among women worldwide. It is a disease in which malignant (cancer) cells form in the tissues of the breast and become deadly when they metastasize, spreading to oth...

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Adding exercise to rosuvastatin treatment: influence on C-reactive protein, monocyte toll-like receptor 4 expression, and inflammatory monocyte (CD14+CD16+) population

Cited by 38 publications

References 41 publications

The Influence of Atorvastatin and Rosuvastatin in Atherosclerosis on the Parameters of Cellular Immunity and in Vitro Leucocyte Activation

The Influence of Atorvastatin and Rosuvastatin in Atherosclerosis on the Parameters of Cellular Immunity and in Vitro Leucocyte Activation

Innate Immune Responses in the Geriatric Population

Potential Mechanisms behind Physical Exercise vs. Epigenetic Regulation for Preventing Breast Cancer

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