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1.南京中医药大学中西医结合学院,南京 210023
2.南京中医药大学骨伤修复与重建新技术实验室,南京 210023
3.南京中医药大学附属苏州市中医院骨伤科,江苏 苏州 215008
4.泰州市姜堰中医院脊柱骨伤科,江苏 泰州 225300
5.南京中医药大学附属医院放射科,南京 210023
硕士研究生。研究方向:中药防治脊柱退行性疾病。E-mail:baixue2021202102@163.com
副主任医师,博士生导师,博士。研究方向:中医药防治脊柱退行性疾病的临床与基础研究。E-mail:okdoctor@163.com
收稿日期:2023-11-29,
修回日期:2024-04-18,
录用日期:2024-04-23,
纸质出版日期:2024-05-30
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白雪,孙孝先,郭杨,等.益气活血方对大鼠腰椎间盘突出的影响及机制[J].中国药房,2024,35(10):1186-1192.
BAI Xue,SUN Xiaoxian,GUO Yang,et al.Effects and mechanism of Yiqi huoxue decoction on lumbar disc herniation in rats[J].ZHONGGUO YAOFANG,2024,35(10):1186-1192.
白雪,孙孝先,郭杨,等.益气活血方对大鼠腰椎间盘突出的影响及机制[J].中国药房,2024,35(10):1186-1192. DOI: 10.6039/j.issn.1001-0408.2024.10.06.
BAI Xue,SUN Xiaoxian,GUO Yang,et al.Effects and mechanism of Yiqi huoxue decoction on lumbar disc herniation in rats[J].ZHONGGUO YAOFANG,2024,35(10):1186-1192. DOI: 10.6039/j.issn.1001-0408.2024.10.06.
目的
2
探讨益气活血方(YQHX)对大鼠腰椎间盘突出的影响及机制。
方法
2
大鼠随机分为假手术组、模型组、核因子κB(NF-κB)抑制剂组(QNZ组,1 mg/kg)、YQHX组(9.1 g/kg)及联合组(YQHX+QNZ组,剂量同各单药组),每组10只。除假手术组外,其余各组大鼠建立腰椎间盘突出症模型,各给药组大鼠腹腔注射QNZ和/或灌胃YQHX,每天给药1次,连续8周。评估各组大鼠椎间盘突出严重程度,观察椎间盘组织形态学变化、髓核细胞自噬变化,检测血清中肿瘤坏死因子α(TNF-α)水平、椎间盘组织中B细胞淋巴瘤2/腺病毒E1B相互作用蛋白3(BNIP3)、苄氯素1(Beclin-1)阳性细胞百分比,核因子κB(NF-κB) p65磷酸化水平,肿瘤坏死因子受体相关因子2(TRAF-2)、TRAF-3、BNIP3、微管相关蛋白轻链3B(LC3B)蛋白表达水平,以及NF-κB p65、LC3B、p62、BNIP3及Beclin-1 mRNA表达水平。
结果
2
与模型组比较,YQHX组大鼠椎间盘Pfirrmann分级评分显著降低,病理损伤减轻;髓核细胞自噬小体数量增加;血清中TNF-α水平和椎间盘组织中p62 mRNA表达水平均显著降低;椎间盘组织中BNIP3、Beclin-1阳性细胞百分比,NF-κB p65磷酸化水平,TRAF-2、TRAF-3、BNIP3、LC3B蛋白表达水平,NF-κB p65、LC3B、BNIP3、Beclin-1 mRNA表达水平均显著升高(
P
<0.05)。加入QNZ可部分逆转YQHX组上述指标的变化。
结论
2
YQHX可能通过激活NF-κB信号通路促进大鼠椎间盘自噬水平升高,减轻炎症反应,延缓腰椎间盘突出症进展。
OBJECTIVE
2
To investigate the effects and mechanism of Yiqi huoxue decoction (YQHX) on lumbar disc herniation in rats.
METHODS
2
Rats were randomly divided into sham operation group, model group, NF-κB inhibitor group (QNZ group, 1 mg/kg), YQHX group (9.1 g/kg) and combination group (YQHX+QNZ group, the same dose as each single drug group), with 10 rats in each group. Except for sham operation group, lumbar disc herniation model of rats was induced in other groups; administration groups were given QNZ intraperitoneally or/and YQHX intragastrically, once a day, for 8 consecutive weeks. The severity of intervertebral disc herniation was evaluated in each group; the pathological changes of intervertebral discs and the changes of autophagy of nucleus pulposus cells were all observed; the level of tumor necrosis factor-α (TNF-α) in serum, and the ratios of Bcl-2/adenovirus E1B interacting protein 3 (BNIP3) and Beclin-1 positive cells in intervertebral disc tissues were detected; the phosphorylation of nuclear factor-κB (NF-κB) p65, the expressions of tumor necrosis factor receptor-associated factor-2 (TRAF-2), TRAF-3, BNIP3 and LC3B protein, and mRNA expressions of NF-κB p65, LC3B, p62, BNIP3 and Beclin-1 were determined.
RESULTS
2
Compared with model group, Pfirrmann grading score decreased significantly, the pathological injury of intervertebral disc tissue was relieved in YQHX group; the number of autophagosomes in nucleus pulposus cells increased; serum level of TNF-α and mRNA expression of p62 in intervertebral disc tissue decreased significantly; the ratios of BNIP3 and Beclin-1 positive cells, the phosphorylation of NF-κB p65, the expressions of TRAF-2, TRAF-3, BNIP3 and LC3B protein as well as the mRNA expressions of NF-κB p65, LC3B, BNIP3 and Beclin-1 decreased significantly in intervertebral disc tissues (
P
<0.05). The changes of above indexes in YQHX group were reversed partly in YQHX+QNZ group.
CONCLUSIONS
2
YQHX promotes the elevation of autophagy level of intervertebral discs, slows down the inflammatory response and the progression of lumbar disc herniation by activating the NF-κB signaling pathway.
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