本文探讨了夏枯草粗多糖（PVCP）对镉诱导肾小管上皮细胞RPTEC/TERT1炎症反应的调节作用。CCK-8法测定氯化镉与PVCP对RPTEC/TERT1作用24 h后的细胞存活率。将细胞设置为对照组（空白培养基）、模型组（8 μmol/L氯化镉）及PVCP高、中、低剂量干预组（200、100、50 μg/mL PVCP加8 μmol/L氯化镉）。测定细胞内超氧化物歧化酶（SOD）、过氧化氢酶（CAT）酶活力的变化，细胞上清液中白细胞介素-6（IL-6）、白细胞介素-1β（IL-1β）、白细胞介素-18（IL-18）、肿瘤坏死因子α（TNF-α）的水平以及细胞内iκB及p65表达水平。结果显示，夏枯草样品中多糖含量为2.14%。氯化镉剂量依赖性抑制RPTEC/TERT1细胞活力。与对照组相比，镉处理组细胞内SOD、CAT含量显著升高（p<0.01），IL-6、IL-1β、IL-18及TNF-α表达水平分别升高了9.53倍、8.80倍、10.86倍和1.17倍（p<0.01）。同时，NF-κB信号通路关键蛋白iκB及p65的表达显著升高（p<0.05）。与模型组相比，PVCP干预组SOD及CAT活力下降（p<0.01），IL-1β、IL-6、TNF-α、IL-18分泌下降（p<0.01），iκB及p65的表达降低（p<0.05）。结果表明，PVCP可改善镉诱导的RPTEC/TERT1细胞炎症反应，该效应可能与其抗氧化能力及对NF-κB信号通路的抑制有关。

The regulatory effects of crude polysaccharides extracted from Prunella vulgaris L. (PVCP) on cadmium-induced inflammatory responses in human renal proximal tubule epithelial cells RPTEC/TERT1 were investigated. Cell counting kit-8 (CCK-8) assay was used to detect the survival rate of RPTEC/TERT1 cells after cadmium or PVCP treatment for 24h. Control group (blank culture medium), model group (8 μmol/L cadmiumchloride) and high-，medium- and low-dose groups of PVCP (8 μmol/L cadmiumchloride +200, 100, 50 μg/mL PVCP)were set in this study. The catalase (CAT) and superoxide dismutase (SOD) activities of RPTEC/TERT1 cells, interleukin (IL)-6, IL-1β, IL-18 and tumor necrosis factor (TNF)-α levels in the supernatant and the protein expression levels of iκB and p65 were evaluated. The results showed that the content of polysaccharides in Prunella vulgaris L. sample was 2.14%. The viability of RPTEC/TERT1 cells was significantly inhibited by cadmium chloride in a dose-dependent manner. In addition, the activities of SOD and CAT of RPTEC/TERT1 cells in the cadmium treated group were significantly decreased (p＜0.01)in comparison with control group, while the expression levels of IL-6, IL-1β, IL-18 and TNF-α wereincreased by 9.53 times, 8.80 times, 10.86 times and 1.17 times, respectively (p<0.01). Meanwhile, the expression levels of key proteins iκB and p65 in NF-κB signaling pathway were significantly increased (p<0.05). Compared to the model group, the activities of SOD and CAT were significantly increased (p＜0.01), while IL-1β, IL-6, TNF-α and IL-18 as well as iκB and p65 were significantly decreased (p<0.05) after PVCP treatment. In conclusion, PVCP could ameliorate cadmium-induced inflammation in RPTEC/TERT1 cells, and its anti-inflammatory effect may be related to antioxidant response and inhibition of NF-κB signaling pathway.

国家重点研发计划项目（2018YFC1603101）；广州市科技计划项目（201803010107）；广东省重点领域研发计划项目（2019B020210002）；国家自然科学基金资助项目（81872642）