目的 對(duì)阿膠的補(bǔ)血、抗疲勞、抗氧化、止血的功效進(jìn)行研究。方法 將SD大鼠隨機(jī)分為對(duì)照組、模型組、生血丸1.5 g/kg組和阿膠1.500、0.750、0.375 g/kg組，ig給藥14 d，采用乙酰苯肼聯(lián)合環(huán)磷酰胺制備大鼠復(fù)合血虛模型，檢測(cè)大鼠游泳力竭時(shí)間，進(jìn)行血液學(xué)及血清丙二醛（MDA）、超氧化物歧化酶（SOD）水平檢測(cè)，考察阿膠的補(bǔ)血、抗疲勞、抗氧化作用；ICR小鼠隨機(jī)分為對(duì)照組、生血丸3 g/kg組和阿膠3.00、1.50、0.75 g/kg組，ig給藥15 d，以毛細(xì)管法和剪尾法測(cè)定凝血時(shí)間（CT）和出血時(shí)間（BT）；采用肝素化大鼠出血模型考察阿膠的止血作用及可能機(jī)制。結(jié)果 在復(fù)合血虛模型中，與模型組比較，阿膠1.50、0.75 g/kg能夠明顯延長大鼠游泳時(shí)間（P<0.05、0.01），體力耗竭速度減慢；1.5 g/kg可升高紅細(xì)胞計(jì)數(shù)（RBC）、血紅蛋白（HGB）濃度、紅細(xì)胞壓積（HCT）、淋巴細(xì)胞（LYM）百分比（P<0.05）；1.500、0.750、0.375 g/kg顯著降低血清中MDA的含量（P<0.01）。在正常血液功能檢測(cè)中，3.00、1.50 g/kg阿膠能夠顯著縮短CT和BT（P<0.05），改善率最大可達(dá)29.4%。在肝素化出血模型中，1.5 g/kg阿膠可顯著逆轉(zhuǎn)肝素化所致的凝血酶原時(shí)間（PT）延長（P<0.05）。結(jié)論 阿膠具有"升紅"、提高免疫力、抗氧化、抗疲勞的藥理活性，且能夠拮抗血液的肝素化，對(duì)凝血因子可能具有活化作用，起到止血收斂的作用。

Objective To evaluate the antifatigue, anti-oxidant and hemostatic effects, and to explore the potential hemostatic mechanism of Asini Corii Colla (ACC). Methods The SD rats were randomly divided into control group, model group, Shengxue Pills (1.5 g/kg) group and ACC (1.500, 0.750, and 0.375 g/kg) group, and rats were ig administered for 14 d. Rat model of complex blood deficiency induced by acetyl phenylhydrazine (APH) and cyclophosphamide (CTX) was used to detect rat exhaustive swimming time, take hematological examination, Malondialdehyde (MDA), and superoxide dismutase (SOD) level detection, which aims to explore the hematopoiesis, antifatigue and anti-oxidant effects of ACC. ICR mice were randomly divided into control group, Shengxue Pills (3 g/kg) group and ACC (3, 1.50, and 0.75 g/kg) group, and they were ig administered for 15 d. Clotting time (CT) and the bleeding time (BT) in normal mice were measured using methods of tail cutting and glass capillary. The heparinized bleeding model in rats was established for investigating the possible mechanism of hemostasis. Results In the complex model of blood deficiency, the ACC of 1.50 and 0.75 g/kg dose significantly prolonged the swimming time of model rats (P<0.05 and 0.01), delayed physical exhaustion time, increased the RBC, Lymphocyte, and HGB significantly (P<0.05), and decreased the content of MDA in serum significantly (P<0.05). In the normal blood function tests, the ACC significantly reduced the BT and CT (P<0.05), and the maximum improving rate was up to 29.4%. In hemorrhage model of heparinized blood, the ACC markedly reversed the prolonged prothrombin time (PT) induced by heparin (P<0.05). Conclusions The ACC have the pharmacological effects of hematopoiesis, immunity enhancement, anti-oxidation, and antifatigue. Additionally, the ACC could also antagonize the blood heparinization by the activation of coagulation factors in a certain extent, so ACC may play a role in hemostasis.

國家科技重大專項(xiàng)（2015ZX09501004）；天津市科技計(jì)劃項(xiàng)目（16PTGCCX00090）；山東省重點(diǎn)研發(fā)計(jì)劃（2016GGH4514）；國家中藥標(biāo)準(zhǔn)化項(xiàng)目（ZYBZH-Y-SD-31）