Inhibitory effects of astragaloside IV on diabetic peripheral neuropathy in rats

2006 ◽  
Vol 84 (6) ◽  
pp. 579-587 ◽  
Author(s):  
Junxian Yu ◽  
Yindi Zhang ◽  
Shi Sun ◽  
Jianping Shen ◽  
Jun Qiu ◽  
...  
Keyword(s):  
Peripheral Neuropathy ◽  
Aldose Reductase ◽  
Blood Glucose Concentration ◽  
Motor Nerve ◽  
Diabetic Rats ◽  
Threshold Temperature ◽  
Radical Scavenger ◽  
Protective Mechanism ◽  
Myelinated Fiber ◽  
Astragaloside Iv

Astragaloside IV (AGS-IV), a new glycoside of cycloartane-type triterpene isolated from the root of Astragalus membranaceus (Fisch.) Bunge, has been used experimentally for its potent immune-stimulating, anti-inflammatory, and antioxidative actions. A recent study has shown AGS-IV to be an aldose-reductase inhibitor and a free-radical scavenger. This study examined the effects of AGS-IV on motor nerve conduction velocity (MNCV), tailflick threshold temperature, biochemical indexes, and the histology of the sural nerve after diabetes was induced in rats with 75 mg/kg streptozotocin (STZ). AGS-IV (3, 6, 12 mg/kg, twice a day) was administered by oral gavage for 12 weeks after diabetes was induced. Compared with control (nondiabetic) rats, obvious changes in physiological behaviors and a significant reduction in sciatic MNCV in diabetic rats were observed after 12 weeks of STZ administration. Morphological analysis showed that AGS-IV suppressed a decrease in myelinated fiber area, an increase in myelinated fiber density, and an increase in segmental demyelination in diabetic rats. The protective mechanism of AGS-IV involved a decrease in declining blood glucose concentration and HbA1C levels, and an increase in plasma insulin levels. AGS-IV increased the activity of glutathione peroxidase in nerves, depressed the activation of aldose reductase in erythrocytes, and decreased the accumulation of advanced glycation end products in both nerves and erythrocytes. Moreover, AGS-IV elevated Na+,K+-ATPase activity in both the nerves and erythrocytes of diabetic rats. These results indicate that AGS-IV exerts protective effects against the progression of peripheral neuropathy in STZ-induced diabetes in rats through several interrelated mechanisms.

Comparison of the Effects of Prophylactic and Therapeutic Administrations on Peripheral Neuropathy in Streptozotocin-Diabetic Rats with Gliclazide or Methylcobalamin

2018 ◽  
Vol 128 (10) ◽  
pp. 635-643
Author(s):  
Hongping Yao ◽  
Juanyi Feng ◽  
Qiaowei Zheng ◽  
Youxia Wei ◽  
Guangde Yang ◽  
...  
Keyword(s):  
Peripheral Neuropathy ◽  
Diabetic Neuropathy ◽  
Enzyme Activities ◽  
Diabetic Peripheral Neuropathy ◽  
Motor Nerve ◽  
Diabetic Rats ◽  
Antioxidative Enzyme ◽  
Prophylactic Administration ◽  
Antioxidative Enzyme Activities ◽  
Therapeutic Administration

Abstract Objective To observe the differences in curative effects between prophylactic and therapeutic administrations of Gliclazide (GLZ) or Methylcobalamin (MCA) on diabetic peripheral neuropathy in rats. Methods GLZ (25 mg/kg/day) or MCA (175 μg/kg/day) was orally administrated prophylactically to streptozotocin-induced diabetic rats for 8 weeks before diabetic peripheral neuropathy developed or administrated therapeutically after diabetic peripheral neuropathy developed, respectively. The motor nerve conduction velocities (MNCV), aldose reductase (AR) activities, the polyol contents and antioxidative enzyme activities in the sciatic never tissues were determined. The morphology of sciatic never tissues was observed. Results In comparison to vehicle, most of the changes in the sciatic nerves of the diabetic rats (e. g., delayed MNCV, altered/damaged nerve structure, enhanced AR activity, increased polyol contents, altered Cu, Zn-superoxide dismutase, glutathione-peroxidase activities, and elevated malondialdehyde level) were significantly ameliorated by prophylactic administration with either GLZ or MCA. In contrast, only few of above-mentioned parameters were alleviated in DPN rats by therapeutic administration with GLZ or MCA as compared to vehicle. The curative effects of GLZ or MCA prophylactic administration on MNCV, AR activity, polyol contents and antioxidative enzyme activities were markedly stronger than therapeutic administration. Conclusion Prophylactic administration of GLZ or MCA was superior to the therapeutic administration in alleviation of diabetic neuropathy in STZ-rats, suggesting that pharmacotherapy should be initiated at a much earlier stage before diabetic neuropathy developed, but not at a later stage after never damage reached.

Slowing of peripheral motor nerve conduction was ameliorated by aminoguanidine in streptozocin-induced diabetic rats

1996 ◽  
Vol 134 (4) ◽  
pp. 467-473 ◽  
Author(s):  
Yosuke Miyauchi ◽  
Hisataka Shikama ◽  
Toshiyuki Takasu ◽  
Hideaki Okamiya ◽  
Masako Umeda ◽  
...  
Keyword(s):  
Sciatic Nerve ◽  
Atpase Activity ◽  
Nerve Conduction ◽  
Renal Cortex ◽  
Motor Nerve ◽  
Diabetic Rats ◽  
Myelinated Fiber ◽  
Peripheral Tissues ◽  
Motor Nerve Conduction ◽  
Peripheral Motor

Miyauchi Y, Shikama H, Takasu T, Okamiya H, Umeda M, Hirasaki E, Ohhata I, Nakayama H, Nakagawa S. Slowing of peripheral motor nerve conduction was ameliorated by aminoguanidine in streptozocin-induced diabetic rats. Eur J Endocrinol 1996:134:467–73. ISSN 0804–4643 The aims of this study were to investigate the effect of aminoguanidine (AG) on slowing of motor nerve conduction velocity (MNCV) of the sciatic nerve in streptozocin-induced diabetic rats and to assess its mechanism of action. The MNCV of the sciatic nerve was measured electrophysiologically in diabetic rats treated with and without AG for 16 weeks. To elucidate the action of AG, morphological lesion and abnormality of polyol pathway metabolism in the nerve were examined and tissue levels of advanced glycosylation end-products (AGE) were determined as an indicator of AGE accumulation in tissue. Diabetic rats were treated with AG at three doses of 10, 25 and 50 mg/kg for 16 weeks. Myelinated fiber morphometry and nerve Na+,K+-ATPase activity were determined. The AGE levels in renal cortex were measured by a specific ELISA. Aminoguanidine dose-dependently ameliorated slowing of MNCV 16 weeks after the treatment without changing body weight or blood glucose levels. No difference in myelinated fiber morphometry or Na+,K+-ATPase activity with or without AG treatment was detected in diabetic rats. Diabetes increased the AGE level in the renal cortex by six times compared to non-diabetic rats, and AG reduced the rise in the AGE level by 40%. The MNCV was inversely correlated with the AGE levels. We conclude that improvement of conduction slowing by AG in experimental diabetes may be through decreasing the AGE level in the peripheral tissues. Aminoguanidine may have a therapeutic potential in controlling diabetic peripheral neuropathy. Hisataka Shikama, Endocrinology and Metabolic Disease Research Laboratory, Yamanouchi Pharmaceutical Co., Ltd., 21 Miyukigaoka, Tsukuba, Ibaraki 305 Japan

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