Intervention effect of Qizhi Tongqiao Capsules on the contractile function of the corpus cavernosum smooth muscle cells aging model in rats induced by D-galactose

YAN Junfeng; JIANG Zhuocheng; YE Miaoyong; YU Jiandi; MA Limin; ZHANG Chunhe; ZHAO Fan

doi:10.16025/j.1674-1307.2025.01.003

您当前的位置：

首页 >

文章列表页 >

Intervention effect of Qizhi Tongqiao Capsules on the contractile function of the corpus cavernosum smooth muscle cells aging model in rats induced by D-galactose

更新时间：2025-01-24

- Intervention effect of Qizhi Tongqiao Capsules on the contractile function of the corpus cavernosum smooth muscle cells aging model in rats induced by D-galactose
- Beijing Journal of Traditional Chinese Medicine Vol. 44, Issue 1, Pages: 12-18(2025)
- 作者机构：
  
  1.浙江大学医学院附属浙江医院泌尿外科，杭州 310030
  2.南通大学附属医院泌尿外科，南通 226001
  3.温州医科大学附属温岭医院泌尿外科，温岭 317500
  4.云南省中医医院泌尿男科，昆明 650021
- 作者简介：
- 基金信息：
- DOI：10.16025/j.1674-1307.2025.01.003
  CLC：
- Published：25 January 2025，
  
  Received：28 September 2024，
- 稿件说明：
移动端阅览
YAN JUNFENG, JIANG ZHUOCHENG, YE MIAOYONG, et al. Intervention effect of Qizhi Tongqiao Capsules on the contractile function of the corpus cavernosum smooth muscle cells aging model in rats induced by D-galactose. [J]. Beijing journal of traditional chinese medicine, 2025, 44(1): 12-18.
DOI：

YAN JUNFENG, JIANG ZHUOCHENG, YE MIAOYONG, et al. Intervention effect of Qizhi Tongqiao Capsules on the contractile function of the corpus cavernosum smooth muscle cells aging model in rats induced by D-galactose. [J]. Beijing journal of traditional chinese medicine, 2025, 44(1): 12-18. DOI： 10.16025/j.1674-1307.2025.01.003.

摘要

目的

探讨芪蛭通窍胶囊（QTC）对D-半乳糖诱导的原代大鼠阴茎海绵体平滑肌细胞（CCSMC）衰老模型收缩功能的影响及作用机制。

方法

体外分离、培养SD大鼠CCSMC，制备QTC含药血清。将CCSMC随机分为正常组、模型组、干预组。正常组常规培养，模型组、干预组在此基础上加入灭菌后的30 mg/mL的D-半乳糖溶液干预48 h制备衰老模型。正常组、模型组培养基中加入20% FBS，干预组培养基中加入20%的QTC含药血清，继续培养48 h。β-半乳糖苷酶染色实验观察CCSMC衰老状态，胶原凝胶收缩实验检测CCSMC收缩率，Western blotting法检测CCSMC表型相关蛋白［α-平滑肌激动蛋白（α-SMA）、结蛋白（Desmin）、I型胶原蛋白（Collagen I）、波形蛋白（Vimentin）］和Janus激酶2（JAK2）、信号转导和转录激活因子3（STAT3）蛋白表达。

结果

与正常组比较，模型组衰老阳性细胞数量多（

0.01）。与模型组比较，干预组阳性细胞数量少（

0.01）。与正常组比较，模型组CCSMC收缩率低（

0.01）。与模型组比较，干预组CCSMC收缩率高（

0.01）。与正常组比较，模型组CCMSC中α-SMA、Desmin、Collagen I、Vimentin、磷酸化JAK2（p-JAK2）/JAK2、磷酸化STAT3（p-STAT3）/STAT3表达高（

0.01）。与模型组比较，干预组CCMSC中α-SMA、Desmin、Collagen I、Vimentin、p-JAK2/JAK2、p-STAT3/STAT3表达低（

0.01）。

结论

QTC可促进衰老CCSMC表型变化，提高其收缩功能，其机制可能与JAK2/STAT3信号通路有关。

Abstract

Objective

To investigate the effect of Qizhi Tongqiao Capsules （QTC） on the contractile function of D-galactose-induced primary corpus cavernosum smooth muscle cells （CCSMC） aging model in rats and to explore the mechanism of action.

Methods

CCSMCs were isolated and cultured from SD rats in vitro， and QTC-containing serum was prepared. CCSMCs were randomly divided into the normal group， model group， and intervention group. The normal group was cultured conventionally， while the model and intervention groups were treated with sterilized 30 mg/mL D-galactose solution for 48 hours to induce aging. The normal and model groups were cultured with 20% FBS， while the intervention group was cultured with 20% QTC-containing serum for another 48 hours. The aging state of CCSMCs was observed by β-galactosidase staining， and the contractile rate was measured by a collagen gel contraction assay. The expression of phenotypic proteins ［α-smooth muscle actin （α-SMA）， desmin， collagen I， vimentin］， Janus kinase 2 （JAK2）， and signal transducer and activator of transcription protein 3 （STAT3） was detected by Western blot.

Results

Compared with the normal group， the model group exhibited a significantly higher number of positive cells （

0.01）. Compared with the model group， the intervention group showed a significantly lower number of positive cells （

0.01）. The contractile rate of CCSMCs in the model group was significantly lower than that of the normal group （

0.01）. Compared with the model group， the intervention group exhibited a significantly higher contractile rate （

0.01）. The expression levels of α-SMA， desmin， collagen I， vimentin， phosphorylated JAK2 （p-JAK2）/JAK2， and phosphorylated STAT3 （p-STAT3）/STAT3 were significantly higher in the model group than in the normal group （

0.01）. The intervention group showed significantly lower expression levels of α-SMA， desmin， collagen I， vimentin， p-JAK2/JAK2， and p-STAT3/STAT3 than the model group （

0.01）.

Conclusion

QTC can promote phenotypic changes in aging CCSMCs and enhance their contractile function. The mechanism may be related to the modulation of the JAK2/STAT3 signaling pathway.

关键词

难治性勃起功能障碍衰老相关勃起功能障碍芪蛭通窍胶囊阴茎海绵体平滑肌细胞收缩功能Janus激酶2/信号转导和转录激活因子3信号通路

Keywords

refractory erectile dysfunctionaging-related erectile dysfunctionQizhi Tongqiao Capsulescorpus cavernosum smooth muscle cellscontractile functionJAK2/STAT3 signaling pathway

references

赵凡,李海松,张春和,等.难治性勃起功能障碍中西医结合防治策略述评[J].中华中医药杂志,2023,38(9):4013-4021.

MOREIRA ED JR, LBO CF, DIAMENT A, et al. Incidence of erectile dysfunction in men 40 to 69 years old: results from a population-based cohort study in Brazil[J]. Urology, 2003,61(2):431-436.

WANG W, FAN J, HUANG G, et al. Meta-analysis of prevalence of erectile dysfunction in mainland china: evidence based on epidemiological surveys[J]. Sex Med, 2017,5(1):e19-e30.

LU Y, FAN S, CUI J, et al. The decline in sexual function, psychological disorders (anxiety and depression) and life satisfaction in older men: A cross-sectional study in a hospital-based population[J].Andrologia,2020,52(5):e13559.

ANTONIO L, WU FCW, MOORS H, et al. Erectile dysfunction predicts mortality in middle-aged and older men independent of their sex steroid status[J]. Age Ageing, 2022,51(4):afac094.

LIU K, SUN T, LUAN Y, et al. Berberine ameliorates erectile dysfunction in rats with streptozotocin-induced diabetes mellitus through the attenuation of apoptosis by inhibiting the SPHK1/S1P/S1PR2 and MAPK pathways[J]. Andrology, 2022,10(2):404-418.

CHEN L, STAUVLI SE, SCHNEIFER MP, et al. Phosphodiesterase 5 inhibitors for the treatment of erectile dysfunction: a trade-off network meta-analysis[J]. Eur Urol, 2015,68(4):674-680.

CLAVIJO RI, KOHN TP, KOHN JR, et al. Effects of low-intensity extracorporeal shockwave therapy on erectile dysfunction: a systematic review and meta-analysis[J]. J Sex Med, 2017,14(1):27-35.

FERRINI MG, GONZALEZ-CADAVID NF, RAJFER J. Aging related erectile dysfunction-potential mechanism to halt or delay its onset[J]. Transl Androl Urol, 2017,6(1):20-27.

MACDONALD SM, BURNETT AL. Physiology of erection and pathophysiology of erectile dysfunction[J]. Urol Clin North Am, 2021,48(4):513-525.

FERRER JE, VELEZ JD, HERRERA AM. Age-related morphological changes in smooth muscle and collagen content in human corpus cavernosum[J]. J Sex Med, 2010,7(8):2723-2728.

孙曼婷,高东晓,罗瑛，等.衰老细胞与衰老：靶向衰老细胞药物研究进展[J].中国中西医结合杂志,2022,42(12):1525-1530.

颜德馨,胡泉林,王平平,等.气虚血瘀是人体衰老的主要机制[J].中国医药学报,1989,4(2):10-12,79.

AMAN KF， ZAKARIA R. D-Galactose-induced accelerated aging model： an overview［J］. Biogerontology， 2019，20（6）：763-782.

KHACHIGIAN LM, BLACK BL, FERDINANDY P, et al. Transcriptional regulation of vascular smooth muscle cell proliferation, differentiation and senescence: Novel targets for therapy[J]. Vascul Pharmacol, 2022,146:107091.

LIN MJ, HU SL, TIAN Y, et al. Targeting vascular smooth muscle cell senescence: a novel strategy for vascular diseases[J]. J Cardiovasc Transl Res, 2023,16(5):1010-1020.

WICHER SA, ROOS BB, TESKE JJ, et al. Aging increases senescence, calcium signaling, and extracellular matrix deposition in human airway smooth muscle[J]. PLoS One, 2021,16(7):e0254710.

CHAPPELL J, HARMAN JL, NARASIMHAN VM, et al. Extensive proliferation of a subset of differentiated, yet plastic, medial vascular smooth muscle cells contributes to neointimal formation in mouse injury and atherosclerosis models[J]. Circ Res, 2016,119(12):1313-1323.

焦琳茜,徐旭英,郭卉,等.舒脉胶囊干预血管内皮细胞-平滑肌细胞共培养模型的作用机制研究[J].北京中医药,2023,42(7):708-715.

颜俊锋,赵凡,周海永,等.红景天苷通过PDGFR/STAT3信号通路调控大鼠阴茎海绵体平滑肌细胞表型转化的实验研究[J].中华男科学杂志,2022,28(2):107-113.

周海永,颜俊锋,赵凡,等.老年大鼠膀胱排尿功能及平滑肌细胞表型变化[J].浙江医学,2020,42(24):2614-2618,2717.

赵凡,叶妙勇,张春和,等.膀胱平滑肌细胞表型转化和膀胱功能障碍的相关研究进展[J].中华实验外科杂志,2023,40(9):1879-1884.

PHILIPS RL, WANG Y, CHEON H, et al. The JAK-STAT pathway at 30: Much learned, much more to do[J]. Cell, 2022,185(21):3857-3876.

SONG HT, CUI Y, ZHANG LL, et al. Ruxolitinib attenuates intimal hyperplasia via inhibiting JAK2/STAT3 signaling pathway activation induced by PDGF-BB in vascular smooth muscle cells[J]. Microvasc Res, 2020,132:104060.

ZHOU W, WANG W, YUAN XJ, et al. The effects of RBP4 and Vitamin D on the proliferation and migration of vascular smooth muscle cells via the JAK2/STAT3 signaling pathway[J]. Oxid Med Cell Longev, 2022:3046777.

YAN JF, HUANG WJ, ZHAO JF, et al. The platelet-derived growth factor receptor/STAT3 signaling pathway regulates the phenotypic transition of corpus cavernosum smooth muscle in rats[J].PLoS One,2017,12(2):e0172191.

Views

下载量

CSCD

Alert me when the article has been cited

提交

Tools

Publicity Resources

Pathogenesis and therapeutic methods of diabetic erectile dysfunction based on collateral disease theory

Related Author

MA Jianxiong

YE Miaoyong

LI Haisong

ZHANG Chunhe

WANG Bin

MA Limin

ZHAO Fan

LI Yueqing

Related Institution

Department of Nephropathy， The First Affiliated Hospital of Zhejiang Chinese Medical University

Urology Surgery， The Affiliated Wenling Hospital of Wenzhou Medical University， Wenling

Department of Andrology， Dongzhimen Hospital Affiliated to Beijing University of Chinese Medicine

Department of Andrology， The First Affiliated Hospital of Yunnan University of Chinese Medicine

Urology Surgery， Affiliated Hospital of Nantong University

⁰