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摘要：
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摘要：目的 探索紫檀芪（pterostilbene，PTE）对细菌脂多糖（lipopolysaccharide，
LPS）诱导的人HL-7702肝脏细胞损伤的作用及机制。方法 建立LPS诱导的人HL-7702
细胞炎症损伤模型，分别使用不同浓度（1 μg/ml、5 μg/ml、10 μg/ml、20 μg/ml、
40 μg/ml、60 μg/ml、80 μg/ml、100 μg/ml，6 h）的LPS诱导肝细胞损伤，选择合适的
作用浓度。分别使用10 μg/ml、15 μg/ml、20 μg/ml的PTE预处理HL-7702模型细胞。
利用MTT法检测各组细胞存活率。利用Western blot检测各组细胞的B淋巴细胞瘤-2
（B-cell lymphoma-2，BcL-2）、B淋巴细胞瘤-2相关的蛋白质X（BcL2-asssociated X，
Bax）、核因子-κB（nuclear factor kappa-B，NF-κB）、肿瘤坏死因子-α（tumor necrosis
factor-α，TNF-α）、白细胞介素-6（interleukin-6，IL-6）的蛋白表达水平。结果 与正
常对照组相比，100 μg/ml LPS损伤组细胞A值显著下降（0.54 ± 0.01 vs 0.38 ± 0.02），
Bax（0.36 ± 0.07 vs 0.87 ± 0.09）、NF-κB（0.40 ± 0.01 vs 0.90 ± 0.02）、TNF-α（0.35 ±
0.07 vs 0.90 ± 0.04）及IL-6（0.30 ± 0.04 vs 0.73 ± 0.09）蛋白表达水平显著上升，BcL-2
蛋白表达下调（0.81 ± 0.08 vs 0.32 ± 0.07），差异均具有统计学意义（P均＜ 0.05）。
与100 μg/ml LPS组细胞相比，15 μg/ml PTE预处理组A值显著增加（0.34 ± 0.01 vs 0.46 ±
0.01）、Bax（0.87 ± 0.09 vs 0.61 ± 0.09）、NF-κB（0.90 ± 0.02 vs 0.73 ± 0.06）、TNF-α
（0.90 ± 0.04 vs 0.66 ± 0.06）及IL-6（0.73 ± 0.09 vs 0.53 ± 0.03）蛋白表达水平显著下
降，BcL-2蛋白表达上调（0.32 ± 0.07 vs 0.68 ± 0.02），差异均有统计学意义（P均＜
0.05）。结论 PTE可抑制LPS诱导的肝细胞凋亡，减少炎性介质产生，其机制可能与抑
制NF-κB信号转导通路的激活有关。
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Abstract: Objective To evaluate the effects and mechanisms of pterostilbene (PTE) on
lipopolysaccharide (LPS) -induced liver injury of HL-7702. Methods HL-7702 cells were
stimulated with different concentration (1 μg/ml, 5 μg/ml, 10 μg/ml, 20 μg/ml, 40 μg/ml,
60 μg/ml, 80 μg/ml, 100 μg/ml) of LPS for 6 h to select the appropriate concentration in
order to establish the inflammation injury model. HL-7702 cells were treated with PTE (10 μg/ml,
15 μg/ml, 20 μg/ml) after inflammation injury model was established. MTT assay was
performed to detect the cell viability and the levels of B-cell lymphoma-2 (BcL-2), BCL2-
associated X (Bax), nuclear factor kappa-B (NF-κB), tumor necrosis factor-α (TNF-α) and
interleukin-6 were evaluated by Western blot. Results Compared with blank control group,
A values of 100 μg/ml LPS group decreased significantly (0.54 ± 0.01 vs 0.38 ± 0.02), while
Bax (0.36 ± 0.07 vs 0.87 ± 0.09), NF-κB (0.40 ± 0.01 vs 0.90 ± 0.02), TNF-α (0.35 ± 0.07 vs
0.90 ± 0.04) and IL-6 (0.30 ± 0.04 vs 0.73 ± 0.09) levels increased significantly, BcL-2 level
decreased significantly, the differences were statistically significant (all P ＜ 0.05). Compared
with 100 μg/ml LPS group, A values of 15 μg/ml PTE group increased significantly (0.34 ± 0.01
vs 0.46 ± 0.01), while Bax (0.87 ± 0.09 vs 0.61 ± 0.09), NF-κB (0.90 ± 0.02 vs 0.73 ± 0.06),
TNF-α (0.90 ± 0.04 vs 0.66 ± 0.06) and IL-6 (0.73 ± 0.09 vs 0.53 ± 0.03) levels decreased
significantly, BcL-2 level increased significantly, the differences were statistically significant
(all P ＜ 0.05). Conclusions PTE alleviates LPS-induced HL-7702 cells injury by reducing
inflammatory response and inhibiting cell apoptosis, the mechanism may be related to the
inhibition of the activation of NF-κB signaling transduction pathway
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