巴戟天多糖通过靶向lncRNA XIST调控糖酵解-焦亡延缓小鼠骨关节炎软骨细胞退变

doi:10.12122/j.issn.1673-4254.2025.12.02

南方医科大学学报 ›› 2025, Vol. 45 ›› Issue (12): 2541-2550.doi: 10.12122/j.issn.1673-4254.2025.12.02

• • 上一篇

巴戟天多糖通过靶向lncRNA XIST调控糖酵解-焦亡延缓小鼠骨关节炎软骨细胞退变

付长龙¹^,²(), 陈若岚¹, 徐诗淇³, 游锦欣¹, 林晴³, 黄艳峰¹^,²()

^1.福建中医药大学中西医结合学院中西医结合研究院，福建福州 350122
^2.福建省中西医结合老年性疾病重点实验室，福建福州 350122
^3.福建中医药大学中医骨伤学院，福建福州 350122

收稿日期:2025-06-17 出版日期:2025-12-20 发布日期:2025-12-22
通讯作者: 黄艳峰 E-mail:993001232@qq.com;banglongnet@126.com
作者简介:付长龙，副研究员，E-mail: 993001232@qq.com
基金资助:
国家自然科学基金(82474532);福建省中青年教师教育科研项目(JAT231042);福建省自然科学基金(2024J01138);福建中医药大学校管课题(X2023024)

Morinda officinalis polysaccharide delays osteoarthritis mouse chondrocyte degeneration by modulating the glycolysis-pyroptosis axis via targeting the lncRNA XIST

Changlong FU¹^,²(), Ruolan CHEN¹, Shiqi XU³, Jinxin YOU¹, Qing LIN³, Yanfeng HUANG¹^,²()

^1.Research Institute of Integrative Medicine, School of Integrative Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou 350122, China
^2.Fujian Provincial Key Laboratory of Integrative Medicine for Geriatric Diseases, Fuzhou 350122, China
^3.College of Traditional Chinese Medicine Orthopedics, Fujian University of Traditional Chinese Medicine, Fuzhou 350122, China

Received:2025-06-17 Online:2025-12-20 Published:2025-12-22
Contact: Yanfeng HUANG E-mail:993001232@qq.com;banglongnet@126.com
Supported by:
National Natural Science Foundation of China(82474532)

摘要/Abstract

摘要：

目的探讨巴戟天多糖（MOP）延缓骨关节炎（OA）软骨细胞退变的作用机制。方法提取4周龄C57BL/6小鼠软骨细胞，经纯化培养、鉴定后，采用白介素-1β（IL-1β）诱导软骨细胞退变模型，随机将细胞分为对照组、IL-1β、MOP-L（1、2、4、6、8、10 mg/mL）组，通过CCK-8法筛选MOP最佳干预条件；Western blotting检测MOP不同剂量对丙酮酸激酶M2（PKM2）、半胱天冬酶1（caspase-1）和消皮素D（GSDMD）的蛋白表达；采用荧光原位杂交技术（FISH）法观察各组软骨细胞中lncRNA XIST的表达；对lncRNA XIST进行过表达与敲减，随机将细胞分为Control、IL-1β、IL-1β+MOP、IL-1β+oe/sh-XIST、IL-1β+oe/sh-XIST+MOP组，采用real-time PCR检测各组软骨细胞糖酵解调控因子葡萄糖转运体1（GLUT1）、己糖激酶2（HK2）、PKM2、乳酸脱氢酶A（LDHA）、6磷酸果糖2激酶/果糖-2，6-二磷酸酶3（PFKFB3），焦亡调控因子核苷酸结合寡聚结构域样受体蛋白3（NLRP3）、caspase-1、GSDMD的mRNA水平；流式细胞术观察各组软骨细胞的凋亡率；甲苯胺蓝染色观察各组软骨细胞糖胺聚糖表达情况；Western blotting检测各组软骨细胞糖酵解和焦亡调控因子蛋白表达。结果镜下结果显示，第2代软骨细胞状态良好，II型胶原蛋白染色呈阳性表达，IL-1β诱导后，细胞数量稍减，触角增多并皱缩，II型胶原蛋白着色减少，PKM2、caspase-1和GSDMD蛋白表达增加；当MOP不同剂量干预退变软骨细胞后，其活力值增加，以MOP-M（4 mg/mL）干预24 h最明显，且PKM2、caspase-1和GSDMD蛋白表达降低（P<0.05）。lncRNA XIST主要分布在软骨细胞核中，与对照组相比较，IL-1β组的软骨细胞lncRNA XIST荧光表达增加；与IL-1β组相比较，IL-1β+MOP组和MOP组软骨细胞lncRNA XIST荧光表达减少；与IL-1β+MOP组相比较，MOP组软骨细胞lncRNA XIST荧光表达减少（P<0.05）。lncRNA XIST过表达后促进糖酵解和焦亡相关因子的mRNA及蛋白表达（P<0.05），且与IL-1β刺激具有协同效应。MOP干预可逆转IL-1β或IL-1β+oe-XIST诱导的上述因子表达上调（P<0.05）。当lncRNA XIST敲减后能抑制软骨细胞凋亡和软骨细胞糖胺聚糖的表达，降低糖酵解（HK2、PKM2、PFKFB3）和焦亡（caspase-1、NLRP3、GSDMD）蛋白表达（P<0.05），MOP干预显示出与XIST敲减相似的保护效果，当两者联合使用时效果更明显（P<0.05）。结论本研究表明MOP通过靶向lncRNA XIST调控糖酵解-焦亡，显著抑制IL-1β诱导的软骨细胞退变，为OA治疗提供新策略。

关键词: 巴戟天多糖, 骨关节炎, 退变软骨细胞, 细胞焦亡, 糖酵解, lncRNA XIST

Abstract:

Objective To investigate the mechanism by which Morinda officinalis polysaccharide (MOP) delays osteoarthritis chondrocyte degeneration. Methods In primary cultures of chondrocytes from 4-week-old C57BL/6 mice, the effects of IL-1β and MOP treatment at different concentrations on cell viability were assessed with CCK-8 assay. The treated cells were examined for protein expressions of PKM2, caspase-1, and GSDMD using Western blotting and for XIST expression using fluorescence in situ hybridization (FISH). In IL-1β-induced mouse chondrocytes, the effects of MOP, transfection for XIST overexpression or knockdown, and MOP treatment after the transfection were tested by detecting mRNA levels of GluT1, HK2, PKM2, LDHA, PFKFB3, NLRP3, caspase-1, and GSDMD; flow cytometry, Western blotting, and toluidine blue staining were used to analyze chondrocyte apoptosis, expressions of glycolysis and pyroptosis regulators, and glycosaminoglycan expression. Results The second-passage chondrocytes showed good viability and positive collagen II staining. IL-1β induction caused degenerative morphological changes of the cells, decreased collagen II expression, and upregulated cellular expressions of PKM2, caspase-1, and GSDMD proteins. MOP treatment (especially at 4 mg/mL) significantly enhanced cell viability and reduced HK2, PKM2, caspase-1 and GSDMD expressions in IL-1β‑induced mouse chondrocytes. XIST was localized predominantly in the nuclei of the chondrocytes, and its expression increased significantly in IL-1β‑treated cells, and was attenuated by MOP treatment. XIST overexpression synergized with IL-1β to upregulate mRNA and protein expressions of glycolysis- and pyroptosis-related factors in the chondrocytes, and such effects were obviously attenuated by MOP. Conversely, XIST knockdown significantly inhibited chondrocyte apoptosis and glycosaminoglycan expression, and down-regulated glycolysis- and pyroptosis-related proteins. MOP treatment exhibited similar protective effects to XIST knockdown, and their combination significantly augmented these protective effects. Conclusions MOP mitigates IL-1β‑induced mouse chondrocyte degeneration by modulating glycolysis and pyroptosis via targeting XIST.

Key words: Morinda officinalis polysaccharide, osteoarthritis, degenerated chondrocytes, pyroptosis, glycolysis, lncRNA XIST

付长龙, 陈若岚, 徐诗淇, 游锦欣, 林晴, 黄艳峰. 巴戟天多糖通过靶向lncRNA XIST调控糖酵解-焦亡延缓小鼠骨关节炎软骨细胞退变[J]. 南方医科大学学报, 2025, 45(12): 2541-2550.

Changlong FU, Ruolan CHEN, Shiqi XU, Jinxin YOU, Qing LIN, Yanfeng HUANG. Morinda officinalis polysaccharide delays osteoarthritis mouse chondrocyte degeneration by modulating the glycolysis-pyroptosis axis via targeting the lncRNA XIST[J]. Journal of Southern Medical University, 2025, 45(12): 2541-2550.

图/表 8

表1 PCR引物序列

Tab.1 Primer sequences for RT-qPCR

Gene	Primer sequences	Produet length (bp)
GLUT1	F:5'-ACCATCTTGGAGCTGTTCCG-3' R:5'-GCCTTCTCGAAGATGCTCGT-3'	131
HK2	F:5'-CCAGAGCATCCTCCTCAAGT-3' R:5'-GGTCTTCATAGCCACAAGTCATC-3'	173
PKM2	F:5'-AGGCTGCCATCTACCACTTG-3' R:5'-CCAGACTTGGTGAGCACGAT-3'	148
LDHA	F:5'-CAGACTTGGCTGAGAGCATAATG-3' R:5'-CCTTCACAACATCCGAGATTCC-3'	147
PFKFB3	F:5'-CAGGATCTTGTCCAACGCCT-3' R:5'-AGGCTAGTAGGCAGCGTAGA-3'	103
NLRP3	F:5'-TCCCAGACACTCATGTTGCC-3' R:5'-GTCCAGTTCAGTGAGGCTCC-3'	116
Caspase-1	F:5'-ACTGACTGGGACCCTCAAGT-3' R:5'-GCAAGACGTGTACGAGTGGT-3'	111
GSDMD	F:5'-TTAATTGAGGCGGCAGACTTC-3' R:5'-CGATGTTCACCAGTATCTGTTGT-3'	109
GAPDH	F:5'-TGGAAAGCTGTGGCGTGATG-3' R:5'-TACTTGGCAGGTTTCTCCAGG-3'	189

图1 软骨细胞培养、诱导与鉴定

Fig.1 Primary culture, induction, and identification of mouse chondrocytes. A: Morphology of primary chondrocytes. B: Morphology of the second-passage chondrocytes. C: Positive expression of collagen II protein. D: Negative expression of collagen II protein. E: Morphology of chondrocytes induced by IL-1β. F: IL-1β induces positive expression of collagen II protein.

图3 MOP不同剂量对PKM2、caspase-1和GSDMD的蛋白表达影响

Fig.3 Effect of different concentrations of MOP on protein expressions of PKM2, caspase-1 and GSDMD in mouse chondrocytes. Data are presented as Mean±SD (n=3). *P<0.05 vs Control group, #P<0.05 vs IL-1β group.

图5 MOP对IL-1β诱导后lncRNA XIST过表达软骨细胞中GLUT1、HK2、PKM2、LDHA、PFKFB3、NLRP3、caspase-1、GSDMD的mRNA水平影响

Fig.5 Effect of MOP on mRNA levels of GLUT1, HK2, PKM2, LDHA, PFKFB3, NLRP3, caspase-1, and GSDMD in mouse chondrocytes overexpressing XIST with IL-1β treatment. Data are presented as Mean±SD (n=3). *P<0.05 vs Control group; #P<0.05 vs IL-1β group; ▲P<0.05 vs IL-1β+oe-XIST group.

图6 MOP对IL-1β诱导后lncRNA XIST过表达软骨细胞中HK2、PKM2、PFKFB3、NLRP3、caspase-1、GSDMD的蛋白表达影响

Fig.6 Effect of MOP on protein expressions of HK2, PKM2, PFKFB3, NLRP3, caspase-1, and GSDMD in mouse chondrocytes overexpressing XIST with IL-1β treatment. Data are presented as Mean±SD (n=3). *P<0.05 vs Control group; #P<0.05 vs IL-1β group; ▲P<0.05 vs IL-1β+oe-XIST group.

图7 MOP对IL-1β诱导后lncRNA XIST敲减软骨细胞凋亡影响

Fig.7 Effect of MOP on apoptosis in mouse chondrocytes with XIST knockout and IL-1β treatment. Data are presented as Mean±SD (n=3). *P<0.05 vs Control group; #P<0.05 vs IL-1β group; ▲P<0.05 vs IL-1β+sh-XIST group.

图8 MOP对IL-1β诱导后lncRNA XIST敲减软骨细胞糖胺聚糖的影响

Fig.8 Effect of MOP on glycosaminoglycan expression in mouse chondrocytes with XIST knockout and IL-1β treatment (Scale bar=100 μm).

图9 MOP对IL-1β诱导后lncRNA XIST敲减软骨细胞中HK2、PKM2、PFKFB3、caspase-1、NLRP3、GSDMD的蛋白表达影响

Fig.9 Effect of MOP on protein expressions of HK2, PKM2, PFKFB3, NLRP3, caspase-1, and GSDMD in mouse chondrocytes with XIST knockout and IL-1β treatment. Data are presented as Mean±SD (n=3). *P<0.05 vs Control group; #P<0.05 vs IL-1β group; ▲P<0.05 vs IL-1β+sh-XIST group.

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巴戟天多糖通过靶向lncRNA XIST调控糖酵解-焦亡延缓小鼠骨关节炎软骨细胞退变

Morinda officinalis polysaccharide delays osteoarthritis mouse chondrocyte degeneration by modulating the glycolysis-pyroptosis axis via targeting the lncRNA XIST

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