杠柳次苷调控STAT3抑制人胰腺癌细胞系增殖和侵袭

doi:10.11958/20260112

天津医药 ›› 2026, Vol. 54 ›› Issue (7): 673-681.doi: 10.11958/20260112

• 细胞与分子生物学 • 下一篇

杠柳次苷调控STAT3抑制人胰腺癌细胞系增殖和侵袭

闫奇¹(), 陈晨², 解维敏¹^,^△()

¹ 神木市医院肝胆外科（邮编719300）
² 西安交通大学第一附属医院胆道外科

收稿日期:2026-01-07 修回日期:2026-02-28 出版日期:2026-07-15 发布日期:2026-07-13
通讯作者: ^△E-mail：312027454@qq.com
作者简介:闫奇（1985），男，主治医师，主要从事胰腺、胆道相关疾病方面研究。E-mail：Dor09Qiqi@163.com
基金资助:
陕西省重点研发计划(2020SF-070)

Periplocymarin regulates STAT3 to inhibit proliferation and invasion of human pancreatic cancer cell lines

YAN Qi¹(), CHEN Chen², XIE Weimin¹^,^△()

¹ Department of Hepatobiliary Surgery, Shenmu Hospital, Shenmu 719300, China
² Department of Biliary Tract Surgery, the First Affiliated Hospital of Xi’an Jiaotong University

Received:2026-01-07 Revised:2026-02-28 Published:2026-07-15 Online:2026-07-13
Contact: ^△E-mail：312027454@qq.com

闫奇, 陈晨, 解维敏. 杠柳次苷调控STAT3抑制人胰腺癌细胞系增殖和侵袭[J]. 天津医药, 2026, 54(7): 673-681.

YAN Qi, CHEN Chen, XIE Weimin. Periplocymarin regulates STAT3 to inhibit proliferation and invasion of human pancreatic cancer cell lines[J]. Tianjin Medical Journal, 2026, 54(7): 673-681.

摘要/Abstract

摘要：

目的探究杠柳次苷（PPM）对人胰腺癌细胞系增殖和侵袭的影响，并分析其是否通过调控信号转导和转录激活因子3（STAT3）发挥抗癌作用。方法（1）体外实验：将SW1990细胞分为对照组，0.05、0.1、0.2 PPM组（分别用0.05、0.1和0.2 μmol/L PPM培养48 h），NC-oe+0.2 PPM组（转染NC-oe，0.2 μmol/L PPM培养）和STAT3-oe+0.2 PPM组（转染STAT3-oe，0.2 μmol/L PPM培养）。采用MTT实验及EdU染色检测细胞增殖，TUNEL检测细胞凋亡，Transwell实验检测细胞侵袭。（2）体内实验：将裸鼠随机分为模型组、L-PPM组[1.0 mg/（kg·d） PPM]、H-PPM组[3.0 mg/（kg·d） PPM]、NC-oe+H-PPM组[转染NC-oe，3.0 mg/（kg·d） PPM]和STAT3-oe+H-PPM组[转染STAT3-oe，3.0 mg/（kg·d） PPM]，每组6只，给药周期为28 d。采用HE染色观察肿瘤组织形态，免疫组化检测肿瘤组织p-STAT3、Ki-67和B细胞淋巴瘤（Bcl）-2表达，qRT-PCR检测细胞和肿瘤组织STAT3 mRNA水平。Western blot检测SW1990细胞和肿瘤组织p-STAT3（Tyr705）、STAT3、Bcl-2、Bcl-2相关X蛋白（Bax）、基质金属蛋白酶（MMP）-2和MMP-9蛋白表达。结果（1）体外实验：与对照组比较，0.05、0.1和0.2 PPM组SW1990细胞的STAT3 mRNA和p-STAT3（Tyr705）蛋白水平均降低（P<0.05），相对细胞活力、EdU阳性率、侵袭细胞数量以及Bcl-2、MMP-2和MMP-9蛋白水平均降低（P<0.05），TUNEL阳性率和Bax蛋白水平均升高（P<0.05）。与NC-oe+0.2 PPM组比较，STAT3-oe+0.2 PPM组SW1990细胞的STAT3 mRNA和p-STAT3（Tyr705）蛋白水平均升高（P<0.05），相对细胞活力、EdU阳性率、侵袭细胞数量以及Bcl-2、MMP-2和MMP-9蛋白水平均升高（P<0.05），TUNEL阳性率和Bax蛋白水平均降低（P<0.05）。（2）体内实验：与模型组比较，L-PPM组和H-PPM组裸鼠肿瘤体积、STAT3 mRNA水平、p-STAT3（Tyr705）蛋白水平以及p-STAT3、Ki-67和Bcl-2的阳性率均降低（P<0.05）。与NC-oe+H-PPM组比较，STAT3-oe+H-PPM组裸鼠肿瘤体积、STAT3 mRNA水平、p-STAT3（Tyr705）蛋白水平以及p-STAT3、Ki-67和Bcl-2的阳性率均升高（P<0.05）。结论 PPM具有抗胰腺癌活性，其通过调控STAT3抑制胰腺癌细胞增殖和侵袭。

关键词: 胰腺肿瘤, 细胞系, 肿瘤, 小鼠, 近交BALB C, 杠柳苷, STAT3转录因子, 杠柳次苷

Abstract:

Objective To reveal the effect of periplocymarin (PPM) on the proliferation and invasion of human pancreatic cancer cell lines, and to analyze whether it exerts anti-cancer effects by regulating signal transducer and activator of transcription 3 (STAT3). Methods (1) In vitro experiments: SW1990 cells were divided into the control group, the 0.05 PPM group, the 0.1 PPM group and the 0.2 PPM group (cultured with 0.05, 0.1 and 0.2 μmol/L PPM for 48 h, respectively), the control lentivirus (NC-oe)+0.2 PPM group (NC-oe+0.2 PPM) and the STAT3 overexpression lentivirus (STAT3-oe)+0.2 PPM group (STAT3-oe+0.2 PPM). The control group was cultured with DMEM medium for 48 h. The NC-oe+0.2 PPM group and the STAT3-oe+0.2 PPM group were first transfected with NC-oe and STAT3-oe into SW1990 cells using Lipofectamine 3000, and then the cells were cultured with 0.2 μmol/L PPM for 48 h. Cell viability was detected by MTT, cell proliferation was detected by EdU staining, cell apoptosis was detected by TUNEL, and cell invasion was detected by Transwell assay. (2) In vivo experiments: Nude mice were randomly divided into the model group, the low (L-PPM) group, the high-dose PPM group (H-PPM), the NC-oe+H-PPM group and the STAT3-oe+H-PPM group, with 6 mice in each group. The model group, the L-PPM group and the H-PPM group were subcutaneously injected with normal SW1990 cells. The NC-oe+H-PPM group and the STAT3-oe+H-PPM group were subcutaneously injected with SW1990 cells transfected with NC-oe and STAT3-oe lentivirus, respectively. After 10 days of inoculation, the model group was intraperitoneally injected with normal saline at a dose of 0.1 mL/10 g, the L-PPM and H-PPM groups were intraperitoneally injected with 1.0 and 3.0 mg/(kg·d) PPM solution, respectively. And the NC-oe+H-PPM group and the STAT3-oe+H-PPM group were intraperitoneally injected with 3.0 mg/(kg·d) PPM solution. The administration cycle was 28 days. The morphology of tumor tissue was observed by HE staining. The expressions of p-STAT3, Ki-67 and Bcl-2 in tumor tissue were detected by immunohistochemistry, and the levels of STAT3 mRNA in cells and tumor tissue were detected by qRT-PCR. The protein expression of p-STAT3 (Tyr705), STAT3, Bcl-2, Bax, matrix metalloproteinase (MMP)-2 and MMP-9 in SW1990 cells and tumor tissue were detected by Western blot assay. Results (1) In vitro experiments: compared with the control group, the levels of STAT3 mRNA and p-STAT3 (Tyr705) protein were all decreased in SW1990 cells in the 0.05, 0.1 and 0.2 PPM groups (P<0.05). Relative cell viability, EdU positive rate, the number of invasion cells and the protein levels of Bcl-2, MMP-2 and MMP-9 decreased (P<0.05), while the positive rate of TUNEL and the protein level of Bax both increased (P<0.05). Compared with the NC-oe+0.2 PPM group, the levels of STAT3 mRNA and p-STAT3 (Tyr705) protein in SW1990 cells were increased in the STAT3-oe+0.2 PPM group (P<0.05). Relative cell viability, EdU positive rate, the number of invasion cells and the protein levels of Bcl-2, MMP-2 and MMP-9 increased (P<0.05), while the positive rate of TUNEL and the protein level of Bax both decreased (P<0.05). (2) In vivo experiments: compared with the model group, the tumor volume, STAT3 mRNA level, p-STAT3 (Tyr705) protein level and the positive rates of p-STAT3, Ki-67 and Bcl-2 in nude mice of the L-PPM group and the H-PPM group were all decreased (P<0.05). Compared with the NC-oe+H-PPM group, the tumor volume, STAT3 mRNA level, p-STAT3 (Tyr705) protein level and the positive rates of p-STAT3, Ki-67 and Bcl-2 in nude mice of the STAT3-oe+H-PPM group were all increased (P<0.05). Conclusion PPM has anti-pancreatic cancer activity, which inhibits the proliferation and invasion of pancreatic cancer cells by regulating STAT3.

Key words: pancreatic neoplasms, cell line, tumor, mice, inbred BALB C, Periplocin, STAT3 transcription factor, Periplocymarin

中图分类号:

R735.9

图/表 15

表1 各组SW1990细胞的STAT3 mRNA和p-STAT3（Tyr705）蛋白表达水平比较

Tab.1 Comparison of STAT3 mRNA and p-STAT3 (Tyr705) protein expression levels between six groups of SW1990 cells （n=6，$\stackrel{-}{x}\pm s$）

组别	STAT3 mRNA	p-STAT3（Tyr705）/STAT3
对照组	1.00±0.06	1.00±0.05
0.05 PPM组	0.70±0.06^a	0.65±0.08^a
0.1 PPM组	0.45±0.04^ab	0.43±0.02^ab
0.2 PPM组	0.24±0.02^abc	0.20±0.02^abc
NC-oe+0.2 PPM组	0.23±0.02	0.19±0.02
STAT3-oe+0.2 PPM组	2.25±0.13^d	1.66±0.16^d
F	762.529^＊＊	342.966^＊＊

图1 各组SW1990细胞p-STAT3表达水平比较 A：对照组；B：0.05 PPM组；C：0.1 PPM组；D：0.2 PPM组；E：NC-oe+0.2 PPM组；F：STAT3-oe+0.2 PPM组。图4、6—7同。

Fig.1 p-STAT3 expression levels in each group of SW1990 cells

表2 各组SW1990细胞的相对细胞活力、EdU、TUNEL 阳性率和Bcl-2、Bax蛋白表达水平比较

Tab.2 Comparison of the relative cell viability, EdU positive rate, TUNEL positive rate, and protein expression levels of Bcl-2 and Bax between each group of SW1990 cells （n=6，$\stackrel{-}{x}\pm s$）

组别		相对细胞活力/%		EdU阳性率/%
对照组		100.00±3.23		100.00±5.11
0.05 PPM组		77.81±6.51^a		82.70±6.47^a
0.1 PPM组		60.35±3.62^ab		64.46±4.11^ab
0.2 PPM组		38.46±3.49^abc		43.12±3.57^abc
NC-oe+0.2 PPM组		39.22±2.96		39.93±2.77
STAT3-oe+0.2 PPM组		69.91±4.79^d		68.63±11.78^d
F		183.597^＊＊		78.132^＊＊
组别	TUNEL阳性率/%		Bcl-2/GAPDH		Bax/GAPDH
对照组	4.82±0.32		1.00±0.06		1.00±0.07
0.05 PPM组	15.35±1.26^a		0.81±0.06^a		2.79±0.36^a
0.1 PPM组	26.91±2.56^ab		0.65±0.04^ab		4.25±0.39^ab
0.2 PPM组	34.58±4.22^abc		0.41±0.03^abc		5.11±0.66^abc
NC-oe+0.2 PPM组	35.41±3.76		0.40±0.02		5.28±0.70
STAT3-oe+0.2 PPM组	18.92±2.33^d		0.62±0.05^d		3.53±0.24^d
F	111.874^＊＊		152.983^＊＊		73.371^＊＊

图2 EdU染色检测各组SW1990细胞增殖水平

Fig.2 The proliferation levels of SW1990 cells in each group detected by EdU staining

图3 TUNEL染色检测各组SW1990细胞凋亡水平

Fig.3 The apoptotic levels of SW1990 cells in each group detected by TUNEL staining

图4 各组SW1990细胞Bcl-2和Bax蛋白表达水平比较

Fig. 4 Comparison of Bcl-2 and Bax protein expression levels between each group of SW1990 cells

图5 Transwell实验中结晶紫染色检测各组SW1990细胞侵袭水平

Fig.5 The invasion levels of SW1990 cells in each group detected by crystal violet staining in Transwell assay

图6 各组SW1990细胞MMP-2和MMP-9蛋白表达水平比较

Fig. 6 Comparison of the expression levels of MMP-2 and MMP-9 proteins between each group of SW1990 cells

表3 各组SW1990细胞的侵袭细胞数以及MMP-2和MMP-9蛋白相对水平

Tab.3 The number of invasive cells and the relative levels of MMP-2 and MMP-9 proteins in SW1990 cells of each group （n=6，$\stackrel{-}{x}\pm s$）

组别	侵袭细胞数/个	MMP-2/GAPDH	MMP-9/GAPDH
对照组	128.17±6.91	1.00±0.02	1.00±0.06
0.05 PPM组	107.17±12.02^a	0.79±0.06^a	0.69±0.05^a
0.1 PPM组	79.33±10.61^ab	0.52±0.03^ab	0.55±0.03^ab
0.2 PPM组	49.67±8.04^abc	0.25±0.02^abc	0.31±0.02^abc
NC-oe+0.2 PPM组	53.50±3.02	0.24±0.02	0.29±0.02
STAT3-oe+0.2 PPM组	88.67±3.14^d	0.62±0.03^d	0.59±0.04^d
F	85.943^＊＊	487.081^＊＊	243.020^＊＊

图7 各组小鼠肿瘤组织p-STAT3表达水平比较

Fig.7 p-STAT3 expression levels in tumor tissue of each group of mice

图8 各组小鼠肿瘤组织p-STAT3免疫组化染色

Fig.8 Immunohistochemical staining of p-STAT3 in tumor tissue of each group of mice

表4 各组小鼠肿瘤组织STAT3 mRNA和p-STAT3（Tyr705）蛋白相对水平以及p-STAT3阳性率比较

Tab.4 Comparison of the relative levels of STAT3 mRNA, p-STAT3 (Tyr705) protein and the positive rate of p-STAT3 in tumor tissue between the six groups of mice （n=6，$\stackrel{-}{x}\pm s$）

组别	STAT3 mRNA	p-STAT3（Tyr705）/STAT3	p-STAT3阳性率/%
模型组	1.00±0.06	1.00±0.07	60.38±7.99
L-PPM组	0.66±0.05^a	0.57±0.06^a	37.44±4.61^a
H-PPM组	0.31±0.02^ab	0.26±0.02^ab	20.47±0.96^ab
NC-oe+H-PPM组	0.30±0.03	0.25±0.02	20.42±0.85
STAT3-oe+H-PPM组	2.61±0.19^c	2.17±0.24^c	78.08±5.90^c
F	622.450^＊＊	290.289^＊＊	159.239^＊＊

图9 各组小鼠肿瘤体积和病理学检测 A：瘤体图像；B：肿瘤生长曲线（0 d和7 d肿瘤尚未出现，14、21、28 d时F分别为67.706、164.498、208.867，均P<0.01），a与模型组比较，b与L-PPM组比较，c与NC-oe+H-PPM组比较，P<0.05；C：肿瘤组织HE染色。

Fig. 9 Tumor volume and pathological examination of each group of mice

图10 各组小鼠肿瘤组织Ki-67和Bcl-2表达水平分析

Fig.10 Analysis of the expression levels of Ki-67 and Bcl-2 in tumor tissue of each group of mice

表5 各组小鼠肿瘤组织中Ki-67和Bcl-2的阳性率比较

Tab.5 Comparison of the positive rates of Ki-67 and Bcl-2 in mouse tumor tissue between different groups （n=6，$\stackrel{-}{x}\pm s$）

组别	Ki-67阳性率/%	Bcl-2阳性率/%
模型组	51.15±8.14	67.84±6.57
L-PPM组	36.98±3.93^a	52.98±4.33^a
H-PPM组	19.18±0.86^ab	30.78±1.72^ab
NC-oe+H-PPM组	18.94±1.68	29.49±2.73
STAT3-oe+H-PPM组	44.80±5.50^c	58.47±2.68^c
F	56.125^＊＊	110.005^＊＊

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杠柳次苷调控STAT3抑制人胰腺癌细胞系增殖和侵袭

Periplocymarin regulates STAT3 to inhibit proliferation and invasion of human pancreatic cancer cell lines

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