“…Due to each compound’s antioxidant and anti-inflammatory properties, it is possible to hypothesize that, besides its possible lipid-lowering effects, this combination could positively affect the inflammatory process, a key event in atherosclerotic plaque formation. Changes in the levels of circulating inflammatory marker hs-CRP [ 26 ] and inflammatory cytokines such as interleukin-32 (IL-32) [ 27 , 28 , 29 ] and interleukin-38 (IL-38) [ 30 , 31 ], as well as a variation in the expression of specific circulating inflamma-miRs (miR-21, miR-146a and miR-126) [ 32 ], have been well described in CVDs. For these reasons, we chose to also investigate BruMeChol TM effects on these parameters.…”
Background: Nutraceutical combinations (NCs) against hypercholesterolemia are increasing in the marketplace. However, the availability of NCs without monacolin K is scarce even though the statin-intolerant population needs it. Methods: This study is a parallel-group, randomized, placebo-controlled, double-blind trial. We evaluated the effects of the NC containing phytosterols, bergamot, olive fruits, and vitamin K2 on lipid profile and inflammatory biomarkers in 118 subjects (mean age ± SD, 57.9 ± 8.8 years; 49 men and 69 women) with hypercholesterolemia (mean total cholesterol ± SD, 227.4 ± 20.8 mg/dL) without clinical history of cardiovascular diseases. At baseline and 6 and 12 weeks of treatment, we evaluated lipid profile (total, LDL and HDL cholesterol, and triglycerides), safety (liver, kidney, and muscle parameters), and inflammatory biomarkers such as hs-CRP, leukocytes, interleukin-32, and interleukin-38 and inflammatory-microRNAs (miRs) miR-21, miR-126, and miR-146a. Results: Compared to the placebo, at 6 and 12 weeks, NC did not significantly reduce total cholesterol (p = 0.083), LDL cholesterol (p = 0.150), and triglycerides (p = 0.822). No changes were found in hs-CRP (p = 0.179), interleukin-32 (p = 0.587), interleukin-38 (p = 0.930), miR-21 (p = 0.275), miR-126 (p = 0.718), miR-146a (p = 0.206), myoglobin (p = 0.164), and creatine kinase (p = 0.376). Among the two reported, only one adverse event was probably related to the nutraceutical treatment. Conclusions: The evaluated nutraceutical combination did not change serum lipid profile and inflammatory parameters, at least not with the daily dose applied in the present study.
“…Due to each compound’s antioxidant and anti-inflammatory properties, it is possible to hypothesize that, besides its possible lipid-lowering effects, this combination could positively affect the inflammatory process, a key event in atherosclerotic plaque formation. Changes in the levels of circulating inflammatory marker hs-CRP [ 26 ] and inflammatory cytokines such as interleukin-32 (IL-32) [ 27 , 28 , 29 ] and interleukin-38 (IL-38) [ 30 , 31 ], as well as a variation in the expression of specific circulating inflamma-miRs (miR-21, miR-146a and miR-126) [ 32 ], have been well described in CVDs. For these reasons, we chose to also investigate BruMeChol TM effects on these parameters.…”
Background: Nutraceutical combinations (NCs) against hypercholesterolemia are increasing in the marketplace. However, the availability of NCs without monacolin K is scarce even though the statin-intolerant population needs it. Methods: This study is a parallel-group, randomized, placebo-controlled, double-blind trial. We evaluated the effects of the NC containing phytosterols, bergamot, olive fruits, and vitamin K2 on lipid profile and inflammatory biomarkers in 118 subjects (mean age ± SD, 57.9 ± 8.8 years; 49 men and 69 women) with hypercholesterolemia (mean total cholesterol ± SD, 227.4 ± 20.8 mg/dL) without clinical history of cardiovascular diseases. At baseline and 6 and 12 weeks of treatment, we evaluated lipid profile (total, LDL and HDL cholesterol, and triglycerides), safety (liver, kidney, and muscle parameters), and inflammatory biomarkers such as hs-CRP, leukocytes, interleukin-32, and interleukin-38 and inflammatory-microRNAs (miRs) miR-21, miR-126, and miR-146a. Results: Compared to the placebo, at 6 and 12 weeks, NC did not significantly reduce total cholesterol (p = 0.083), LDL cholesterol (p = 0.150), and triglycerides (p = 0.822). No changes were found in hs-CRP (p = 0.179), interleukin-32 (p = 0.587), interleukin-38 (p = 0.930), miR-21 (p = 0.275), miR-126 (p = 0.718), miR-146a (p = 0.206), myoglobin (p = 0.164), and creatine kinase (p = 0.376). Among the two reported, only one adverse event was probably related to the nutraceutical treatment. Conclusions: The evaluated nutraceutical combination did not change serum lipid profile and inflammatory parameters, at least not with the daily dose applied in the present study.
“…There is a paucity of reports demonstrating direct effects of IL-38 on hypertension but its anti-inflammatory and hyperlipidemia modulating effects may be involved. 31 , 94 IL-38 inhibited human adipocyte differentiation and reduced secretion of inflammatory cytokines, IL-1β and MCP-1, 95 and IL-38 reduction of joint inflammation involved the NF-κB signaling pathway also known to be involved in hypertension. 96 , 97 Macrophages, smooth muscle cells and vascular endothelial cells also release IL-38 under apoptotic conditions and affect the circulatory Bcl-2/Bax/Caspase-3 signaling pathway, attenuating hyperlipidemia.…”
Section: Regulation Of Interleukin-1 Family In Cardiovascular Diseasesmentioning
confidence: 91%
“… 96 , 97 Macrophages, smooth muscle cells and vascular endothelial cells also release IL-38 under apoptotic conditions and affect the circulatory Bcl-2/Bax/Caspase-3 signaling pathway, attenuating hyperlipidemia. 68 , 94 No direct relationship between IL-38 and hypertension has yet been shown but this molecule does seem to ameliorate the disorder ( Figure 2 ). Figure 2 Interleukin 1 family in hypertension.…”
Section: Regulation Of Interleukin-1 Family In Cardiovascular Diseasesmentioning
Inflammatory factors, such as the IL-1 family, are generally acknowledged to be involved in systemic diseases and IL-1α and IL-1β, in particular, have been linked to cardiovascular disease with IL-18, IL-33, IL-36, IL-37 and IL-38 yet to be explored. The current review aims to summarize mechanisms of IL-18, IL-33, IL-36, IL-37 and IL-38 in myocardial infarction, hypertension, arrhythmia, valvular disease and aneurysm and to explore the potential for cardiovascular disease treatment strategies and discuss future directions for prevention and treatment.
“…IL-38 is a newly discovered cytokine in the IL-1 family and plays an important role in a variety of diseases, including but not limited to CNS diseases. [16][17][18][19][20][21][22][23][24] IL-38 is mainly expressed in the brain, heart, lungs, spleen, thymus, tonsils, and skin, and is less distributed in immune-inactive tissues. 25,26 Moreover, its protein is mainly synthesized and secreted by fibroblast-like synoviocytes, keratinocytes, peripheral blood mononuclear cells, and CD19+ B cells.…”
Interleukin (IL)‐38 is a newly discovered cytokine of the IL‐1 family, which binds various receptors (i.e., IL‐36R, IL‐1 receptor accessory protein‐like 1, and IL‐1R1) in the central nervous system (CNS). The hallmark physiological function of IL‐38 is competitive binding to IL‐36R, as does the IL‐36R antagonist. Emerging research has shown that IL‐38 is abnormally expressed in the serum and brain tissue of patients with ischemic stroke (IS) and autism spectrum disorder (ASD), suggesting that IL‐38 may play an important role in neurological diseases. Important advances include that IL‐38 alleviates neuromyelitis optica disorder (NMOD) by inhibiting Th17 expression, improves IS by protecting against atherosclerosis via regulating immune cells and inflammation, and reduces IL‐1β and CXCL8 release through inhibiting human microglial activity post‐ASD. In contrast, IL‐38 mRNA is markedly increased and is mainly expressed in phagocytes in spinal cord injury (SCI). IL‐38 ablation attenuated SCI by reducing immune cell infiltration. However, the effect and underlying mechanism of IL‐38 in CNS diseases remain inadequately characterized. In this review, we summarize the biological characteristics, pathophysiological role, and potential mechanisms of IL‐38 in CNS diseases (e.g., NMOD, Alzheimer's disease, ASD, IS, TBI, and SCI), aiming to explore the therapeutic potential of IL‐38 in the prevention and treatment of CNS diseases.
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