PDF(Pubmed)
Abstract：
UNASSIGNED: Ischemic cardiomyopathy (ICM) with high morbidity and mortality is closely associated with an abnormal equilibrium of circulation selenium levels. The oxidative stress theory is the most accepted theory of selenium causing ischemic cardiomyopathy. However, the role of inflammatory responses in ICM has received limited attention.
UNASSIGNED: This study included 119 subjects, 43 of whom were patients with ICM, and 76 were healthy controls. Blood specimens were collected from subjects and serum levels of inflammatory and oxidative stress indicators and plasma levels of selenium were measured.
UNASSIGNED: When plasma selenium and indicators of inflammation and oxidative stress were compared between groups, plasma selenium levels were significantly lower in the ICM group than in the control group (68.83874 vs 104.39775, p=0.02032), while indicators of inflammation such as tumour necrosis factor-alpha (TNF-α) (79.09773 vs 46.15634, p<0.001), interleukin-6 (IL-6) (49.41484 vs 38.46923, p<0.01) and neutrophil/lymphocyte ratio (3.696574 vs 2.383658, p<0.001) were significantly higher in the ICM group than in the control group (all of these results were statistically different). Additionally, malondialdehyde (MDA), a marker of oxidative stress, was considerably higher in the ICM group than in the control group (61.63078 vs 39.0609, p<0.01). In contrast, there were no significant differences in superoxide dismutase (SOD) levels between groups (p>0.05). The Poisson regression analysis revealed a significant association between selenium and high levels of MDA, IL-6 and TNF-α (p<0.05). Additionally, selenium was negatively connected with SOD levels and the neutrophil/lymphocyte ratio, but this relationship was not statistically significant (p=0.96, 0.15, respectively).
UNASSIGNED: Selenium deficiency is strongly associated with the development of ICM, and with levels of inflammation and oxidative stress in patients with ICM. Selenium can prevent the development and delay the progression of ICM by alleviating inflammatory responses.
UNASSIGNED: This study included 119 subjects, 43 of whom were patients with ICM, and 76 were healthy controls. Blood specimens were collected from subjects and serum levels of inflammatory and oxidative stress indicators and plasma levels of selenium were measured.
UNASSIGNED: When plasma selenium and indicators of inflammation and oxidative stress were compared between groups, plasma selenium levels were significantly lower in the ICM group than in the control group (68.83874 vs 104.39775, p=0.02032), while indicators of inflammation such as tumour necrosis factor-alpha (TNF-α) (79.09773 vs 46.15634, p<0.001), interleukin-6 (IL-6) (49.41484 vs 38.46923, p<0.01) and neutrophil/lymphocyte ratio (3.696574 vs 2.383658, p<0.001) were significantly higher in the ICM group than in the control group (all of these results were statistically different). Additionally, malondialdehyde (MDA), a marker of oxidative stress, was considerably higher in the ICM group than in the control group (61.63078 vs 39.0609, p<0.01). In contrast, there were no significant differences in superoxide dismutase (SOD) levels between groups (p>0.05). The Poisson regression analysis revealed a significant association between selenium and high levels of MDA, IL-6 and TNF-α (p<0.05). Additionally, selenium was negatively connected with SOD levels and the neutrophil/lymphocyte ratio, but this relationship was not statistically significant (p=0.96, 0.15, respectively).
UNASSIGNED: Selenium deficiency is strongly associated with the development of ICM, and with levels of inflammation and oxidative stress in patients with ICM. Selenium can prevent the development and delay the progression of ICM by alleviating inflammatory responses.
摘要：
未经证实：具有高发病率和死亡率的缺血性心肌病（ICM）与循环硒水平的异常平衡密切相关。氧化应激理论是硒引起缺血性心肌病的最被接受的理论。然而,炎症反应在ICM中的作用受到的关注有限.
未经评估：这项研究包括119名受试者，其中43人是ICM患者，76人是健康对照。收集受试者的血液标本，并测量血清中炎症和氧化应激指标的水平以及血浆中的硒水平。
UNASSIGNED：当在组间比较血浆硒和炎症和氧化应激指标时，ICM组的血浆硒水平显着低于对照组（68.83874vs104.39775，p=0.02032），而炎症指标如肿瘤坏死因子-α（TNF-α）（79.09773vs46.15634，p<0.001），白细胞介素-6（IL-6）（49.41484vs38.46923，p<0.01）和中性粒细胞/淋巴细胞比率（3.696574vs2.383658，p<0.001）在ICM组中明显高于对照组（所有这些结果均具有统计学差异）。此外,丙二醛（MDA），氧化应激的标志，ICM组明显高于对照组（61.63078vs39.0609，p<0.01）。相比之下,各组间超氧化物歧化酶(SOD)水平差异无统计学意义(p>0.05)。泊松回归分析显示硒与高MDA水平之间存在显著关联，IL-6和TNF-α(p<0.05)。此外,硒与SOD水平和中性粒细胞/淋巴细胞比率负相关，但这种关系没有统计学意义(分别为p=0.96,0.15).
未经评估：硒缺乏与ICM的发展密切相关，以及ICM患者的炎症和氧化应激水平。硒可以通过减轻炎症反应来预防ICM的发展并延缓其进展。
未经评估：这项研究包括119名受试者，其中43人是ICM患者，76人是健康对照。收集受试者的血液标本，并测量血清中炎症和氧化应激指标的水平以及血浆中的硒水平。
UNASSIGNED：当在组间比较血浆硒和炎症和氧化应激指标时，ICM组的血浆硒水平显着低于对照组（68.83874vs104.39775，p=0.02032），而炎症指标如肿瘤坏死因子-α（TNF-α）（79.09773vs46.15634，p<0.001），白细胞介素-6（IL-6）（49.41484vs38.46923，p<0.01）和中性粒细胞/淋巴细胞比率（3.696574vs2.383658，p<0.001）在ICM组中明显高于对照组（所有这些结果均具有统计学差异）。此外,丙二醛（MDA），氧化应激的标志，ICM组明显高于对照组（61.63078vs39.0609，p<0.01）。相比之下,各组间超氧化物歧化酶(SOD)水平差异无统计学意义(p>0.05)。泊松回归分析显示硒与高MDA水平之间存在显著关联，IL-6和TNF-α(p<0.05)。此外,硒与SOD水平和中性粒细胞/淋巴细胞比率负相关，但这种关系没有统计学意义(分别为p=0.96,0.15).
未经评估：硒缺乏与ICM的发展密切相关，以及ICM患者的炎症和氧化应激水平。硒可以通过减轻炎症反应来预防ICM的发展并延缓其进展。
