Yang Huihai, Li Wei, Wang Lulu, He Xiaofeng, Sun Hang, Zhang Jing
a Department of Traditional Chinese Pharmacology, College of Traditional Chinese Medicine , Jilin Agricultural University , Changchun , China.
b Department of Traditional Chinese Pharmacology, College of Medicine , Changchun Science-Technology University , Changchun , China.
Nat Prod Res. 2018 Aug;32(16):1982-1986. doi: 10.1080/14786419.2017.1356839. Epub 2017 Jul 31.
Our study aimed to investigate the protective role of SDAPR on cisplatin-induced cytotoxicity and its' possible mechanism in HEK293 cells. Cell viability was measured by MTT assay. Oxidative stress (SOD, GSH, LDH and MDA), inflammatory factors (TNF-α and IL-6) and apoptosis-related proteins (caspase-3, Bax, Bcl-2) expression were measured. The apoptotic cells were observed by TUNEL staining. Our study results indicated that non-cytotoxic levels of SDAPR significantly increased viability rate (LD value of cisplatin is 20 μM), which improved antioxidant defence, attenuated apoptosis by decreasing expression levels of cleaved-caspase-3 and Bax, increasing Bcl-2 expression and inhibiting apoptotic positive cells in HEK 293 cells. In addition, SDAPR treatment markedly inhibited the levels of TNF-α and IL-6. In conclusion, Sika deer antler protein, a potential modulator, could alleviate cisplatin-induced cytotoxicity in HEK 293 cells.
我们的研究旨在探讨梅花鹿鹿茸蛋白（SDAPR）对顺铂诱导的细胞毒性的保护作用及其在人胚肾细胞（HEK293）中的可能机制。通过MTT法检测细胞活力。检测氧化应激指标（超氧化物歧化酶、谷胱甘肽、乳酸脱氢酶和丙二醛）、炎症因子（肿瘤坏死因子-α和白细胞介素-6）以及凋亡相关蛋白（半胱天冬酶-3、Bax、Bcl-2）的表达。通过TUNEL染色观察凋亡细胞。我们的研究结果表明，非细胞毒性水平的SDAPR显著提高了细胞活力（顺铂的半数致死剂量为20μM），增强了抗氧化防御能力，通过降低裂解的半胱天冬酶-3和Bax的表达水平、增加Bcl-2的表达以及抑制HEK293细胞中的凋亡阳性细胞来减轻细胞凋亡。此外，SDAPR处理显著抑制了肿瘤坏死因子-α和白细胞介素-6的水平。总之，梅花鹿鹿茸蛋白作为一种潜在的调节剂，可以减轻顺铂诱导的HEK293细胞的细胞毒性。
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