Protective effect of arctigenin in GK rats combined with hypertension macroangiopathy.
- Author:
Qin FENG
;
Bao-cun SUN
;
Wen-kai XIA
- Publication Type:Journal Article
- MeSH:
Animals;
Blood Glucose;
metabolism;
Blood Pressure;
drug effects;
Diabetes Mellitus, Type 2;
complications;
metabolism;
physiopathology;
Diabetic Angiopathies;
etiology;
metabolism;
physiopathology;
prevention & control;
Disease Models, Animal;
Drugs, Chinese Herbal;
administration & dosage;
Furans;
administration & dosage;
Humans;
Hypertension;
etiology;
metabolism;
physiopathology;
prevention & control;
Lignans;
administration & dosage;
Male;
Rats;
Rats, Wistar
- From:
China Journal of Chinese Materia Medica
2015;40(5):957-962
- CountryChina
- Language:Chinese
-
Abstract:
To study the protective effect of Arctigenin in goto-kakizaki (GK) rats combined with hypertension macroangiopathy. Six-week-old GK rats were divided randomly according to blood glucose level into four groups: the model group and low, middle and high dose arctigenin groups (12.5, 25, 50 mg x kg(-1)), with Wistar rats as the normal group. All of GK rats were given high-glucose and high-fat diet. After 16 weeks, GK rats were orally administrated with 10 mg x kg(-1) x d(-1) N-Ω-nitro-L-arginine methyl ester for eight weeks. During the modeling, all of arctigenin groups were orally administrated with different dose of arctigenin twice a day; The model group and the normal group were given solvents. At the beginning, mid-term and end of the experiment, blood glucose was measured. At the end of the experiment, efforts were made to detect blood pressure, collect abdominal aortic blood after anesthesia, fix thoracic aorta after bloodletting to make paraffin sections, observe morphological characteristics and detect the expression of VEGF by immunohistochemistry. According to the results, the blood glucose rose in all GK rats, with no significant difference between the drug group and the model group. At the end of the experiment, the blood pressure significantly increased in GK rats, indicating that Arctigenin could notably reduce the blood pressure in GK rats in a dose-dependent manner. The blood routine test showed increases in both the total white blood cell count and differential blood count, MPV and PDW, abnormal blood platelet parameters and decrease in PLT in GK rats, suggesting that Arctigenin could remarkably reduce the total white blood cell count and differential blood count, MPV and PDW. The thoracic aortic morphological observation revealed obvious endangium lesions in GK rats, demonstrating that Arctigenin could ameliorate the lesion extent. VEGF immumohistochemical staining showed a higher VEGF expression in the model group but lower expression in Arctigenin groups. In conclusion, Arctigenin had a protective effect on aorta in GK rats. Its mechanism may be related to blood pressure lowering, anti-inflammation, improvement in blood platelet function and reduction of VEGF expression.
