| 俞艳艳,王厚东,张秀峰,沈忠.浓缩生长因子联合三七提取物促进慢性肛裂创口修复的作用研究[J].浙江中西医结合杂志,2026,36(2): |
| 浓缩生长因子联合三七提取物促进慢性肛裂创口修复的作用研究 |
| Study on the effect of CGF combined with Panax notoginseng on promoting wound repair in chronic anal fissure |
| 投稿时间：2024-10-12 修订日期：2025-08-26 |
| DOI： |
| 中文关键词: 大鼠 慢性肛裂 三七 浓缩生长因子 TGF-β/Smad信号通路 |
| 英文关键词:Rat Chronic anal fissure Panax notoginseng Concentrated growth factor TGF-β/Smad signaling pathway |
| 基金项目:浙江省中医药科技计划项目 |
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| 摘要点击次数: 85 |
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| 中文摘要: |
| 目的 探究浓缩生长因子（Concentrated growth factor，CGF）结合三七改善慢性肛裂的作用及机制。方法 SD雄性SPF级大鼠30只，按随机数字表法分成对照组（n=6）和慢性肛裂组（n=24）。慢性肛裂组大鼠于肛门后方做一放射状切口，并用冰醋酸连续3d涂抹刺激创面以构建慢性肛裂模型。将造模成功的慢性肛裂组大鼠按随机数字表法分为模型组、CGF组、三七凝胶组、CGF+三七凝胶组，每组6只。CGF组、三七凝胶组、CGF+三七凝胶组分别用CGF凝胶、三七凝胶、CGF+三七凝胶塞肛治疗7d。对照组和模型组不作任何治疗。最后1次给药结束后，观察大鼠一般体征、体质量、热退缩潜伏期变化，同时酶联免疫吸附法检测肛门组织炎症因子水平；组织染色观察肛门组织病理及胶原沉积情况；免疫组化和Western blot观察肛门组织的成纤维标志物和TGF-β/Smad信号通路标志物。结果 与模型组大鼠比较，CGF单独或结合三七治疗后，大鼠一般体征有明显改善，体质量显著增加[（280.17±8.80） g、（275.28±9.37） g、（289.07±10.48） g比（251.87±11.75） g，P<0.01]。热退缩潜伏期结果显示，CGF组、三七凝胶组、CGF+三七凝胶组热退缩潜伏期较模型组显著延长[（13.33±1.69） s、（12.22±1.53） s、（14.72±1.29） s比（9.17±0.86） s，P<0.01或P<0.05]。此外，CGF和三七单独或结合治疗后，大鼠肛门组织炎症得到明显的改善[IL-1β：（60.78±4.76） pg/mL、（71.33±5.84） pg/mL、（38.24±4.39） pg/mL比（97.74±7.62） pg/mL，P<0.01；TNF-α：（138.08±12.16） pg/mL、（123.84±8.44） pg/mL、（52.79±5.37） pg/mL比（178.49±11.50） pg/mL，P<0.01；TGF-β：（272.84±18.62） pg/mL、（288.55±20.27） pg/mL、（337.03±31.21） pg/mL比（221.56±19.70） pg/mL，P<0.01]。病理结果显示，对照组大鼠肛门组织基本正常；模型组大鼠肛门组织损伤严重，表现为细胞排列紊乱，肛周黏膜上皮脱落，大面积炎性细胞浸润，较多细胞坏死，且胶原蛋白沉积增多；而经CGF和三七单独或结合干预后，上述病理损伤得到明显缓解。Western blot分析显示，与模型组相比，CGF组、三七凝胶组、CGF+三七凝胶组肛门组织TGF-β蛋白表达和Smad3磷酸化水平显著增加[TGF-β1：（0.75±0.03）、（0.64±0.01）、（1.17±0.01）比（0.53±0.01），P<0.01；Smad3磷酸化水平：（0.84±0.03）、（0.84±0.02）、（1.13±0.06）比（0.59±0.07），P<0.05]。更为重要的是，与CGF和三七单独用药相比，CGF和三七联合用药具有更好的疗效。结论 CGF结合三七凝胶改善大鼠慢性肛裂溃疡，促进创面组织抗炎和促纤维作用，其机制可能与TGF-β/Smad信号通路的激活有关。 |
| 英文摘要: |
| Objective To investigate the effect and mechanism of concentrated growth factor (CGF) combined with Panax notoginseng on improving chronic anal fissure. Methods Thirty male SD SPF-grade rats were randomly divided into the control group (n=6) and the chronic anal fissure group (n=24) using a random number table. Rats in the chronic anal fissure group underwent a radial incision posterior to the anus, and the wound was continuously stimulated with glacial acetic acid for three days to establish chronic anal fissure models. After successful modeling, the rats in the chronic anal fissure group were randomly divided into the model group, CGF group, Panax notoginseng gel group, and CGF+Panax notoginseng gel group using a random number table, with 6 rats in each group. The CGF group, Panax notoginseng gel group, and CGF+Panax notoginseng gel group were treated with CGF gel, Panax notoginseng gel, and CGF+Panax notoginseng gel, respectively, via rectal administration for 7 days. The control group and model group received no treatment. After the final administration, general physical signs, body weights, and thermal withdrawal latency changes were observed in the rats. Enzyme-linked immunosorbent assay was used to detect inflammatory factor levels in anal tissues. Tissue staining was performed to observe anal tissue pathology and collagen deposition. Immunohistochemistry and Western blot analysis were used to examine fibroblast markers and TGF-β/Smad signaling pathway markers in anal tissues. Results Compared with the rats in the model group, rats treated with CGF and Panax notoginseng gel alone or in combination showed significant improvements in general physical signs and significant increases in body weights [(280.17±8.80) g, (275.28±9.37) g, (289.07±10.48) g vs. (251.87±11.75) g, P<0.01]. The results of the heat withdrawal latency test showed that the heat withdrawal latency in the CGF group, Panax notoginseng gel group, and CGF+Panax notoginseng gel group was significantly prolonged compared with the model group [(13.33±1.69) s, (12.22±1.53) s, (14.72±1.29) s vs. (9.17±0.86) s, P<0.01 or P<0.05]. Additionally, inflammation of the anal tissues in rats treated with CGF and Panax notoginseng gel alone or in combination was significantly improved [IL-1β: (60.78±4.76) pg/mL, (71.33±5.84) pg/mL, (38.24±4.39) pg/mL vs. (97.74±7.62) pg/mL, P<0.01; TNF-α: (138.08±12.16) pg/mL, (123.84±8.44) pg/mL, (52.79±5.37) pg/mL vs. (178.49±11.50) pg/mL, P<0.01; TGF-β: (272.84±18.62) pg/mL, (288.55±20.27) pg/mL, (337.03±31.21) pg/mL vs. (221.56±19.70) pg/mL, P<0.01]. Pathological results showed that the anal tissues of rats in the control group were basically normal; the anal tissues of rats in the model group were severely damaged, characterized by disordered cell arrangement, desquamation of the perianal mucosal epithelium, extensive inflammatory cell infiltration, numerous necrotic cells, and increased collagen deposition; however, after intervention with CGF and Panax notoginseng gel alone or in combination, the aforementioned pathological damages were significantly alleviated. Western blot analysis showed that compared with the model group, the TGF-β protein expression and Smad3 phosphorylation level in the anal tissues of the CGF group, the Panax notoginseng gel group, and the CGF+Panax notoginseng gel group were significantly increased [TGF-β1: (0.75±0.03), (0.64±0.01), (1.17±0.01) vs. (0.53±0.01), P<0.01; Smad3 phosphorylation status: (0.84±0.03), (0.84±0.02), (1.13±0.06) vs. (0.59±0.07), P<0.05]. More importantly, compared with the use of CGF and Panax notoginseng gel alone, the combined use of CGF and Panax notoginseng gel had better therapeutic efficacy. Conclusion CGF combined with Panax notoginseng gel improved chronic anal fissure ulcers in rats and promoted the anti-inflammatory and fibrogenic effects of wound tissues, and the mechanism may be related to the activation of the TGF-β/Smad signaling pathway. |
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