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刘永利,何运恒,卢昌怀,谢芳,李树冬,李前,邵先舫.治伤巴布剂对大鼠急性软组织损伤模型炎症因子及氧化应激的影响[J].湖南中医药大学学报英文版,2022,42(6):893-898.[Click to copy
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| 治伤巴布剂对大鼠急性软组织损伤模型炎症因子及氧化应激的影响 |
| 刘永利,何运恒,卢昌怀,谢芳,李树冬,李前,邵先舫 |
| (海口市中医医院骨伤科, 海南 海口 570216;湖南中医药大学附属常德医院骨伤科, 湖南 常德 415000) |
| 摘要: |
| 目的 观察治伤巴布剂对急性软组织损伤（acute soft tissue injury,ASTI）模型大鼠炎症因子及氧化应激的影响，并分析其作用机制。方法 将24只雄性SD大鼠按照随机数字表法分成3组（正常组、模型组、治伤巴布剂组），每组8只。正常组不造模，其余2组均予以左侧后肢小腿ASTI造模。造模成功后，治伤巴布剂组予治伤巴布剂外敷，其余两组均予等剂量赋形剂外敷，各组均持续外敷24 h。干预后，取各组大鼠左侧后肢小腿损伤中心部位骨骼肌组织，计算肌肉肿胀率（muscle swelling rate,MSR）；采用HE染色观察病理学形态；采用ELISA法检测肿瘤坏死因子-α（tumor necrosis factor-α,TNF-α）、白细胞介素-1β（interleukin-1β,IL-1β）水平；采用生物化学法检测丙二醛（malondialdehyde,MDA）、超氧化物歧化酶（superoxide dismutase,SOD）表达水平。结果 与正常组比较，模型组可见大面积肌细胞排列紊乱，且肌细胞变性、坏死，间质内可见红细胞聚集及大量炎性细胞浸润；模型组MSR及MDA、TNF-α、IL-1β水平明显升高（P<0.01），SOD水平明显降低（P<0.01）。与模型组比较，治伤巴布剂组肌细胞坏死、水肿现象均明显改善，且各类炎性细胞浸润与间质内瘀斑现象均明显减轻；治伤巴布剂组MSR及MDA、TNF-α、IL-1β水平明显著降低（P<0.01），SOD水平明显升高（P<0.01）。结论 治伤巴布剂能降低大鼠ASTI模型骨骼肌组织TNF-α、IL-1β含量水平，减轻炎症反应；可下调样本组织MDA含量水平，上调SOD活性，抑制炎症相关氧化应激水平；降低MSR，从而改善ASTI。 |
| 关键词: 治伤巴布剂 急性软组织损伤 炎症因子 氧化应激 肿瘤坏死因子-α 白细胞介素-1β 丙二醛 超氧化物歧化酶 |
| DOI：10.3969/j.issn.1674－070X.２０22.06.004 |
| Received:January 17, 2022 |
| 基金项目:湖南省中医药科研计划重点项目(2020021);湖南省常德市科技局项目(2019S212);湖南省名中医邵先舫教授工作室建设项目。 |
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| Effect of injury-curing cataplasm on inflammatory factors and oxidative stress in rat model of acute soft tissue injury |
| LIU Yongli,HE Yunheng,LU Changhuai,XIE Fang,LI Shudong,LI Qian,SHAO Xianfang |
| (Department of Orthopaedics and Traumatology of Haikou Hospital of Traditional Chinese Medicine, Haikou, Hainan 570216, China;Department of Orthopaedics and Traumatology, Changde Hospital Affiliated to Hunan University of Chinese Medicine, Changde, Hunan 415000, China) |
| Abstract: |
| Objective To study the effect of injury-curing cataplasm on inflammatory factors and oxidative stress in acute soft tissue injury (ASTI) model, and to analyze its possible mechanism. Methods A total of 24 male SD rats were divided into 3 groups on the basis of random number table method (normal group, model group and injury-curing cataplasm group), with 8 rats in each group. The normal group was not modeled, and ASTI modeling was performed on the left hindlimb and lower leg in the other two groups. After successful modeling, the curing-injury cataplasma group was externally applied with curing-injury cataplasm and the other two groups were externally applied with the same dose of excipient, which lasted for 24 hours. At the end of the drug intervention, skeletal muscle tissue of the center of the left hind leg of each group was collected and muscle swelling rate (MSR) was calculated, and the pathological morphology was observed by HE staining. The levels of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) were determined by ELISA. Biochemical method was used to detect malondialdehyde (MDA) and superoxide dismutase (SOD) expression levels. Results Compared with the normal group, the skeletal muscle tissue of the model group showed a large area of muscle cell disorder, degeneration and necrosis of muscle cells, red blood cells aggregation and a great deal of inflammatory cells infiltration in the stroma; MSR and the levels of MDA, TNF-α and IL-1β were increased (P<0.01), the level of SOD was obviously decreased (P<0.01). Compared with the model group, the necrosis and edema of muscle cells in the injury-curing cataplasm group were obviously improved, and the infiltration of inflammatory cells and ecchymosis in the interstitial were significantly reduced; MSR and the levels of MDA, TNF-α and IL-1β were obviously decreased (P<0.01), the level of SOD increased obviously (P<0.01). Conclusion The injury-curing cataplasm can reduce the content of TNF-α and IL-1β in the skeletal muscle of ASTI model, relieve the inflammatory reaction. It can lower the content of MDA, increase SOD activity, relieve inflammation related oxidative stress, decrease MSR, and thereby improve ASTI. |
| Key words: injury-curing cataplasm acute soft tissue injury inflammation factor oxidative stress tumor necrosis factor-α interleukin-1β malondialdehyde superoxide dismutase |
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