Liu Jian-Hui, Xing Hai-Ting, Wang Yuan-Fang, Luan Hai-Yun, Yang Ming
Department of Neurosurgery, Yantaishan Hospital, Shandong 264001, China.
Zhongguo Zhong Xi Yi Jie He Za Zhi. 2013 Jul;33(7):938-43.
To observe the effect of Panax notoginseng (PN) on pathological features in chronic subdural hematoma (CSDH) rabbits and its mechanisms.
A stable pathological animal model similar to CSDH in humans could be established using subdural injections of small number of blood through a subdural pre-catheter in rabbits. After successful modeling, 18 rabbits were randomly divided into the model group, the low dose PN group (0.125 g/kg), and the high dose PN group (0.250 g/kg), 6 in each group. Normal saline was given to rabbits in the model group, while PN power was given to those in the PN groups by gastrogavage for 6 successive days. Pathologic features of the hematoma outer membrane were observed by HE staining. The activity of SOD and the content of MDA in the hematoma outer membrane were examined by the colorimetric method. Expressions of CD31, CD34, and VEGF in the hematoma outer membrane were observed by immunohistochemical assay. Expressions of VEGF in the peripheral blood and the subdural hematoma were detected by enzyme-linked immunosorbent assay (ELISA). Expressions of VEGFR-1 and VEGFR-2 in the hematoma outer membrane were detected by Western blot.
Compared with the model group, the inflammatory reaction was comparatively lessen and the proliferation of the fibrous tissue was relatively mature in the low and high dose PN groups. The activity of SOD increased (P < 0.05); expressions of CD31 and CD34 were reduced (P < 0.01); VEGF expression in the residual hematoma fluid decreased (P < 0.05) in the high dose PN group. Expressions of VEGF and VEGFR-2 were all reduced in the high and low dose PN groups (P < 0. 05, P < 0.01). Compared with the low dose PN group, expressions of CD31 and CD34 were reduced (P < 0.01), and the VEGFR-2 expression was also reduced (P < 0.05) in the high dose PN group.
PN could promote the fibrous repairing of subdural hematoma in CSDH rabbits. It also lessened inflammation and oxidative injury of the hematoma outer membrane and reduced expressions of VEGF. The pathological angiogenesis could be reduced through influencing VEGFR-2 receptor pathways, which might be an important mechanism.
观察三七对慢性硬膜下血肿（CSDH）家兔病理特征的影响及其机制。
通过家兔硬膜下预先置管注入少量血液，可建立一种与人CSDH相似的稳定病理动物模型。造模成功后，将18只家兔随机分为模型组、低剂量三七组（0.125 g/kg）和高剂量三七组（0.250 g/kg），每组6只。模型组家兔给予生理盐水，三七组家兔连续6天灌胃给予三七粉。采用苏木精-伊红（HE）染色观察血肿外膜的病理特征。采用比色法检测血肿外膜超氧化物歧化酶（SOD）活性和丙二醛（MDA）含量。采用免疫组织化学法观察血肿外膜中CD31、CD34和血管内皮生长因子（VEGF）的表达。采用酶联免疫吸附测定（ELISA）法检测外周血和硬膜下血肿中VEGF的表达。采用蛋白质免疫印迹法检测血肿外膜中血管内皮生长因子受体-1（VEGFR-1）和血管内皮生长因子受体-2（VEGFR-2）的表达。
与模型组相比，低剂量和高剂量三七组的炎症反应较轻，纤维组织增生相对成熟。高剂量三七组SOD活性升高（P < 0.05）；CD31和CD34表达降低（P < 0.01）；残留血肿液中VEGF表达降低（P < 0.05）。低剂量和高剂量三七组VEGF和VEGFR-2表达均降低（P < 0.05，P < 0.01）。与低剂量三七组相比，高剂量三七组CD31和CD34表达降低（P < 0.01），VEGFR-2表达也降低（P < 0.05）。
三七可促进CSDH家兔硬膜下血肿的纤维修复。它还减轻了血肿外膜的炎症和氧化损伤，降低了VEGF的表达。通过影响VEGFR-2受体途径可减少病理性血管生成，这可能是一个重要机制。
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