Abstract：
This study investigated the effects of far-infrared (FIR) irradiation on low-density lipoprotein cholesterol (LDL-C) uptake by human hepatocellular carcinoma G2 (HepG2) cells via the regulation of proprotein convertase subtilisin/kexin type 9 (PCSK9). FIR irradiation for 30 min significantly decreased PCSK9 expression (p < 0.01) in HepG2 cells. FIR irradiation substantially increased the low-density lipoprotein receptor (p < 0.0001) and LDL-C uptake (p < 0.01). Activation of transient receptor potential vanilloid (TRPV) channels mimicked the effects of FIR irradiation, significantly decreasing the protein expression of PCSK9 (p < 0.05). Conversely, inhibition of TRP channels using ruthenium red reversed the reduction in PCSK9 protein expression following FIR irradiation (p < 0.01). The specific activation of TRPV4 using 4α-PDD mimicked the effect of FIR irradiation (p < 0.01), whereas PCSK9 reduction by FIR irradiation was significantly reversed by the inhibition of TRPV4 using RN1734 (p < 0.05). These findings implied that FIR irradiation emitted from a ceramic lamp specifically increased TRPV4 activity. These findings provide insights into a novel therapeutic approach using FIR irradiation for LDL-C regulation and its implications for cardiovascular health.
摘要：
本研究通过调节前蛋白转化酶枯草杆菌蛋白酶/kexin9型（PCSK9），研究了远红外（FIR）照射对人肝细胞癌G2（HepG2）细胞吸收低密度脂蛋白胆固醇（LDL-C）的影响。FIR照射30分钟显著降低HepG2细胞中PCSK9的表达(p<0.01)。FIR照射显著增加低密度脂蛋白受体(p<0.0001)和LDL-C摄取(p<0.01)。瞬时受体电位香草素（TRPV）通道的激活模拟了FIR辐射的作用，显著降低PCSK9的蛋白表达(p<0.05)。相反，使用钌红抑制TRP通道逆转了FIR照射后PCSK9蛋白表达的减少(p<0.01)。使用4α-PDD的TRPV4的特异性激活模拟了FIR照射的效果(p<0.01),而使用RN1734抑制TRPV4显著逆转了FIR照射对PCSK9的减少(p<0.05)。这些发现暗示,从陶瓷灯发射的FIR辐照特别地增加了TRPV4活性。这些发现为使用FIR辐射调节LDL-C的新型治疗方法及其对心血管健康的影响提供了见解。
