This paper studies the protective effect of pine pollen on renal damage in a mouse model of diabetic nephropathy and its mechanism. Fifty adult male C57BL/6J mice were used, and the mouse model of diabetic nephropathy was induced by streptozotocin (STZ). The mice were randomly divided into the control group (n=10) and the STZ model group (n=40). The latter received intraperitoneal injection of a single high dose of 150 mg body weight of STZ dissolved in citrate buffer to induce diabetic nephropathy. The control group were injected with sodium citrate buffer alone. Glucose concentrations in the tail vein blood of the mice were measured 1 week after STZ administration. Only STZ-injected mice with fasting blood glucose concentrations >11.1 mmol/L were included in the diabetic groups. After that, blood glucose and urine protein were detected in 24 hours regularly, and mice with continuing albuminuria were regarded as those with diabetic nephropathy, which totaled 28. The 28 mice were randomly divided into the STZ model group (n=14) and the pine pollen group (n=14). Mice in the pine pollen group were given pine pollen (750 mg) daily. Meanwhile, enema was performed using equal volume of normal saline in the control and STZ model groups. 7 weeks later, plasma glucose concentration, 24 h urinary protein excretion, urine creatinine, serum creatinine and plasma urea nitrogen were detected. The renal tissue was collected to assay the renal weight/body weight ratio and relative level of MDA. Masson staining and Silver staining were performed for histological analyses. The expression of p-p38 and p-ERK in renal cortical tissues was examined using Western Blot. Compared with that in the STZ model group, pine pollen apparently ameliorated renal functional lesion, reduced the renal weight/ body weight ratio and extracellular matrix accumulation. Pine pollen can also reduce the level of MDA and inhibit the activation of p38 and ERK in diabetic kidney. The results showed that pine pollen may reduce oxidative damage of the kidney and extracellular matrix accumulation by inhibiting the phosphorylation level of p38 and ERK in renal cortical tissues.
LI Nan
,
FENG Zhenzhong
,
ZHAO Yan
,
GU Congyou
,
ZHU Bo
,
OU Yurong
. Protective Effect of Pine Pollen on Mice Renal Damage in a Model of Diabetic Nephropathy[J]. Science & Technology Review, 2014
, 32(4-5)
: 95
-99
.
DOI: 10.3981/j.issn.1000-7857.2014.h1.016
[1] Fradkin J E, Cowie C C, Hanlon M C, et al. Celebrating 30 years of research accomplishments of the diabetes control and complications trial/epidemiology of diabetes interventions and complications study[J]. Diabetes, 2013, 62(12): 3963-3967.
[2] 李时珍. 本草纲目[M]. 北京: 人民卫生出版社, 1980: 964. Li Shizhen. Bencao Gangmu[M]. Beijing: The People's Medical Publishing House, 1980: 964.
[3] 潘小玲, 竹剑平. 破壁松花粉的降血糖作用[J]. 中国医院药学杂志, 2006, 26(6): 777-778. Pan Xiaoling, Zhu Jianping. Hypoglycemic activity of pine pollen[J]. Chinese Journal of Hospital Pharmacy, 2006, 26(6): 777-778.
[4] Zhu S S, Ren Y, Zhang M, et al. WldS protects against peripheral neuropathy and retinopathy in an experimental model of diabetes in mice[J]. Diabetologia, 2011, 54(9): 2440-2450.
[5] Sullivan K A, Hayes J M, Wiggin T D, et al. Mouse models of diabetic neuropathy[J]. Neurobiollogy of Disease, 2007, 28(3): 276-285.
[6] Xu B, Chiu J, Feng B, et al. Parp activation and the alteration of vasoactive factors and extracellular matrix protein in retina and kidney in diabetes[J]. Diabetes-Metabolism Research and Reviews, 2008, 24 (5): 404-412.
[7] 冯英, 胡昭, 张佼佼. 糖尿病肾病大鼠肾组织中TSP-1、TGF-β、APP、 VEGF、ColⅠ的表达及意义[J]. 山东医药, 2013, 53(28): 5-8. Feng Ying, Hu Zhao, Zhang Jiaojiao. Expression and significance of TSP- 1, TGF- β, APP, VEGF, Col I in renal tissues of DKD rats[J]. Shandong Medical Journal, 2013, 53(28): 5-8.
[8] Awazu M, Ishikura K, Hida M, et al. Mechanisms of mitogen-activated protein kinase activation in experimental diabetes[J]. Journal of the American Society of Nephrology, 1999, 10(4): 738-745.
[9] Wilmer W A, Dixon C L, Hebert C. Chronic exposure of human mesangial cells to high glucose environments activates the p38 mapk pathway[J]. Kidney International, 2001, 60(3): 858-871.
[10] Sakai N, Wada T, Furuichi K, et al. Involvement of extracellular signal- regulated kinase and p38 in human diabetic nephropathy[J]. American Journal of Kidney Diseases, 2005, 45(1): 54-65.
[11] Rojas- Rivera J, Ortiz A, Egido J. Antioxidants in kidney diseases: The impact of bardoxolone methyl[J]. International Journal of Nephrology, 2012, 2012: 321714-321724.
[12] Ibrahim A S, El-Remessy A B, Matragoon S, et al. Retinal microglial activation and inflammation induced by amadori-glycated albumin in a rat model of diabetes[J]. Diabetes, 2011, 60(4): 1122-1133.