Liang Jun-Qing, Ding Chun-Hua, Ling Yi-Ling, Xu Hai-Bo, Lu Ping, Xian Xiao-Hui
Department of Pathophysiology of Hebei Medical University, Shijiazhuang 050017, China.
Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2007 Aug;23(3):355-8.
To evaluate the roles of puerarin in alleviating the STZ-induced lung injury.
DM model was established by streptozotocin (STZ) intraperitoneal injection to study the injury mechanisms of the lung. SD rats were divided randomly into control group (C group), diabetes group (DM group), diabetes + puerarin group (DM + Pur group). The blood glucose and weight were observed and recorded before and the 20 th, 40 th, 60 thd after administration of saline, STS, STZ+ Pur. Contents of NO and malondialdehyde (MDA) and activity of superoxide dismutase (SOD) were measured in lung tissues. Light microscope (LM), transmission electron microscope (TEM) and immunohistochemical analysis were also used.
(1) Compared with control group, the contents of NO and MDA were increased significantly (P < 0.01), while the activity of SOD reduced (P < 0.05). Compared with DM group, treatment with puerarin inhibited the increase of NO level (P < 0.01), and MDA content began to decline from 40 days after the model was established (P < 0.01), and inhibited the decrease of SOD activity induced by DM (P < 0.01). (2) LM and TEM results showed that alveolar and capillary basement membrane became thick, the number of tiny villus decreased markedly, the quantity of osmiophilic multilamellar body reduced remarkably, hyperplasia was shown in collgen fibre. Puerarin could alleviate above injuries induced by DM. (3) Immunohistochemical staining results showed that mild brown positive stain of NT could be seen in protoplasm of lung tissues. STZ administration induced the expression of NT in the protoplasm of cells, and led to stronger positive signals of NT than that of control group. Treatment with puerarin weakened the positive stain of NT.
(1) DM induced by STZ leads to a significant and sustained increase in blood glucose and obvious lung injury, which may be associated with the overproduction of free radicals. (2) The pathway of NO/ONOO- is one of the injury mechanisms of the lung tissues cells. (3) Puerarin suppresses the expression of NT and elevates the activity of SOD. Thereby, resulting in the reduces of the production of free radicals, which may be one of the mechanisms of its anti-oxidative-injuries.
评估葛根素在减轻链脲佐菌素诱导的肺损伤中的作用。
通过腹腔注射链脲佐菌素(STZ)建立糖尿病模型以研究肺损伤机制。将SD大鼠随机分为对照组(C组)、糖尿病组(DM组)、糖尿病+葛根素组(DM+Pur组)。观察并记录在给予生理盐水、STZ、STZ+Pur之前及给药后第20、40、60天的血糖和体重。检测肺组织中一氧化氮(NO)和丙二醛(MDA)含量以及超氧化物歧化酶(SOD)活性。还采用了光学显微镜(LM)、透射电子显微镜(TEM)和免疫组织化学分析。
(1)与对照组相比,NO和MDA含量显著增加(P<0.01),而SOD活性降低(P<0.05)。与DM组相比,葛根素治疗抑制了NO水平的升高(P<0.01),MDA含量从模型建立后40天开始下降(P<0.01),并抑制了DM诱导的SOD活性降低(P<0.01)。(2)LM和TEM结果显示肺泡和毛细血管基底膜增厚,微绒毛数量明显减少,嗜锇性多层小体数量显著减少,胶原纤维增生。葛根素可减轻DM诱导的上述损伤。(3)免疫组织化学染色结果显示肺组织细胞质中可见轻度棕色阳性染色的神经降压素(NT)。给予STZ诱导细胞细胞质中NT的表达,并导致NT阳性信号比对照组更强。葛根素治疗减弱了NT的阳性染色。
(1)STZ诱导的糖尿病导致血糖显著持续升高和明显的肺损伤,这可能与自由基的过度产生有关。(2)NO/过氧亚硝酸盐途径是肺组织细胞损伤机制之一。(3)葛根素抑制NT的表达并提高SOD的活性。从而导致自由基产生减少,这可能是其抗氧化损伤的机制之一。