紫杉醇/NLS-KALA-SA核定位纳米粒对肺腺癌A549细胞株的抑制作用

目的 观察多肽自组装载体载紫杉醇纳米粒 （NKSP） 及紫杉醇单药对肺腺癌 A549 细胞株的体外抑制作用及可能机制。方法 用噻唑蓝（MTT）法分别检测不同浓度组 NKSP（20、 40、 80、 100 μg/L）、 紫杉醇单药(20、 40、 80、 100 μg/L)作用 24、 48 及 72 h 对 A549 细胞增殖的影响。流式细胞仪检测不加任何药物处理（A）组、 加入 80 μg/L 的多肽自组装纳米粒(NKS)培养液（B）组、 加入 80 μg/L 紫杉醇单药（C）组、 加入含 80 μg/L NKSP（D）组作用 A549 细胞 48 h 及 72 h 时的细胞凋亡率。Western blot 检测 A、 B、 C、 D 组作用 48 h 及 72 h 细胞凋亡相关蛋白 bax、 caspase-3 的表达。结果 紫杉醇单药、 NKSP 均能抑制 A549 的增殖， 紫杉醇单药各组 48 和 72 h 时、 NKSP 单药各组在 72 h 时随浓度递增抑制率也呈递增趋势 （均 P < 0.05）。48 h 时 D 组促 A549 凋亡作用低于 C 组(P < 0.05)， 72 h 强于 C 组(P < 0.05)， 且药物作用 48 h 时 D 组的 bax、 caspase-3 的表达低于 C 组， 而 72 h 时高于 C 组(P < 0.05)。结论 NKS 包裹紫杉醇后可促使载体内的紫杉醇缓慢释放， 与紫杉醇单药相比， 可降低细胞毒性， 延长抗肿瘤作用时间。

Inhibition effects of paclitaxel/NLS-KALA-SA nanoparticles on A549 cell line in vitro

Objective To observe NLS-KALA-SA-PTX (NKSP) for lung adenocarcinoma cell line A549 in vitro with paclitaxel monotherapy, and the mechanism thereof. Methods MTT assay was used to detect A549 cell proliferation influenced by different concentrations of NKSP (20, 40, 80, 100 μg/L) and paclitaxel monotherapy (20, 40, 80, 100 μg/L) for 24 h, 48 h and 72 h.. Subsequent experiments were divided into four groups, namely, group A (without any drug treatment), group B (added polypeptide 80 μg/L of self-assembled nanoparticles, NKS), group C (80 μg/L paclitaxel monotherapy) and group D (80 μg/L NKSP). Flow cytometry was used to detect the cell apoptotic rates after 48 h and 72 h treatment in four groups. Western blot assay was used to analyse the protein expressions of bax and caspase-3 after 48 h and 72 h treatment in four groups. Results Both paclitaxel monotherapy and NKSP can inhibit the proliferation of A549 cells. The inhibitory rates of paclitaxel monotherapy group at 48 h and 72 h and NKSP group at 72 h showed an increasing trend in a dose-dependent manner (P < 0.05). After treatment for 48 hours, the apoptotic rate was significantly higher in D group than that of C group (P < 0.05). But the apoptotic rate at 72 h was lower in D group than that of C group (P < 0.05). The protein expressions of bax and caspase-3 at 48 h were significantl lower in D group than those of C group, which were higher at 72 h in D group than those of C group (P < 0.05). Conclusion Compared to paclitaxel monotherapy group, NKS promotes slow release of paclitaxol, which reduces the cytotoxicity and extends the antitumor effects.