The Immunotherapeutic Effects of Astragalus Polysaccharide in Type 1 Diabetic Mice

Li, Rujiang; Qiu, Shu-Dong; Chen, Hongxia; Tian, Hong; Wang, Hal Xu

doi:10.1248/bpb.30.470

Cited by 61 publications

(46 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Type I diabetes mellitus is due to the destruction of insulin-producing ␤ cells in the pancreatic islets. It is primarily a T cell-mediated autoimmune disease directed against a ␤ cell autoantigen (101). In humans, this is treated with various cocktails of insulin that are designed to release slowly or quickly to try to mimic endogenous patterns.…”

Section: Altered Expression Of Sodium Transporter and Channels In Diamentioning

confidence: 99%

Insulin's impact on renal sodium transport and blood pressure in health, obesity, and diabetes

Tiwari

Riazi²,

Ecelbarger³

2007

American Journal of Physiology-Renal Physiology

111

View full text Add to dashboard Cite

Insulin has been shown to have antinatriuretic actions in humans and animal models. Moreover, endogenous hyperinsulinemia and insulin infusion have been correlated to increased blood pressure in some models. In this review, we present the current state of understanding with regard to the regulation of the major renal sodium transporters by insulin in the kidney. Several groups, using primarily cell culture, have demonstrated that insulin can directly increase activity of the epithelial sodium channel, the sodium-phosphate cotransporter, the sodium-hydrogen exchanger type III, and Na-K-ATPase. We and others have demonstrated alterations in the expression at the protein level of many of these same proteins with insulin infusion or in hyperinsulinemic models. We also discuss how this regulation is perturbed in type I and type II diabetes mellitus. Finally, we discuss a potential role for regulation of insulin receptor signaling in the kidney in contributing to sodium balance and blood pressure. insulin resistance; ENaC; Zucker rats; streptozotocin Overview INSULIN HAS BEEN DEMONSTRATED to increase sodium reabsorption in the proximal tubule (9), the thick ascending limb (78, 102), and the distal tubule including the collecting duct (54, 144), using micropuncture and perfused tubule approaches. Over 10 years ago, Sechi (127), Butlen (30), and colleagues using I 125 -labeled insulin demonstrated binding sites in multiple cell types along the renal tubular epithelium. However, because the kidney expresses other receptors similar to the classic insulin receptor (IR), including the insulin growth factor receptor (IGF) and the IR-related receptor (IRR), the precise nature of the "receptor" that labeled insulin was binding to was not absolutely certain. Nonetheless, more recent studies showed mRNA expression of the classic IR in whole homogenates of the kidney (31, 32,130,132), and our group (150) has recently found IR expression at the protein level using immunoblotting and immunohistochemistry in the proximal tubule, thick ascending limb, and collecting duct. In this review, we discuss studies that have investigated the regulation of the major renal sodium transporters in the kidney by insulin. In addition, we examine how this regulation is altered in insulin resistance, which is a hyperinsulinemic state, as well as in type I and type II diabetes. We also discuss what is known about the regulation of the IR in the kidney, how it is affected by insulin resistance and/or diabetes, and how this might ultimately affect sodium balance and blood pressure.

show abstract

Section: Altered Expression Of Sodium Transporter and Channels In Diamentioning

confidence: 99%

Insulin's impact on renal sodium transport and blood pressure in health, obesity, and diabetes

Tiwari

Riazi²,

Ecelbarger³

2007

American Journal of Physiology-Renal Physiology

111

View full text Add to dashboard Cite

show abstract

“…Diabetic patients and healthcare professions are increasingly considering complimentary and alternative approaches, including by using medicine herbs with combined actions of PPARa and PPARg agonists. Moreover, there are some traditional Chinese medicines, which have been reported for treatment of diabetes, [9][10][11] but there has been inadequate pharmacological research relating to them until now. Taking these facts into account, an attempt was made to find natural drugs with both hypoglycemic and hypolipidemic activities.…”

mentioning

confidence: 99%

Chronic Effects of Berberine on Blood, Liver Glucolipid Metabolism and Liver PPARs Expression in Diabetic Hyperlipidemic Rats

Zhou

Zhang

et al. 2008

Biological & Pharmaceutical Bulletin

137

View full text Add to dashboard Cite

Berberine is one of the main alkaloids of Rhizoma coptidis which has been used as a folk medicine to treat diabetes mellitus for more than 1400 years in China. To investigate the chronic effect of berberine on diabetic hyperlipidemic rats, fasted rats were intraperitoneally injected 35 mg/kg streptozotocin. Diabetic rats were admitted after 2 weeks and given a high-carbohydrate/high-fat diet to induce hyperlipidemia. The rats were divided into 7 groups at the end of week 16: normal and diabetic rats received no drug, 5 treatment groups were administered with either 75, 150, 300 mg/kg berberine, 100 mg/kg fenofibrate or 4 mg/kg rosiglitazone per day for 16 weeks, respectively. The blood glucose, hemoglobin A1c, lipid metabolic parameters and hepatic glycogen and triglyceride were measured, and histopathology and peroxisome proliferator-activated receptors (PPARs) a a/d d/g g expression of liver were determined by hematoxylin eosin and immunohistochemical staining. Berberine reduced diabetic rats' body weight, liver weight and liver to body weight ratio. Berberine restored the increased blood glucose, hemoglobin A1c, total cholesterol, triglyceride, low density lipoprotein-cholesterol, apolipoprotein B and the decreased high density lipoprotein-cholesterol, apolipoprotein AI levels in diabetic rats to near the control ones. Berberine alleviated the pathological progression of liver and reverted the increased hepatic glycogen and triglyceride to near the control levels. Berberine increased PPARa a/d d expression and reduced PPARg g expression in liver of diabetic rat to near the control ones. Berberine improved glucolipid metabolism both in blood and liver in diabetic rats possibly through modulating the metabolic related PPARa a/d d/g g protein expression in liver.

show abstract

“…[18,19] . In recent years, it has been proposed that Astragalus may possess anti-apoptosis potential in peritoneal mesothelial cells [20,21] . In spite of this, the anti-apoptotic effects of Astragalus saponin extract on human peritoneal mesothelial cells during peritoneal carcinomatosishas have not been extensively studied.…”

Section: Astragalus Extract Inhibits Destruction Of Gastric Cancer Cementioning

confidence: 99%

Astragalus extract inhibits destruction of gastric cancer cells to mesothelial cells by anti-apoptosis

Di¹,

Liu²,

Zhang³

et al. 2009

WJG

View full text Add to dashboard Cite

AIM:To determine the inhibitory effect of Astragalus memebranaceushas on gastric cancer cell supernatantinduced apoptosis of human peritoneal mesothelial cells. METHODS:Human peritoneal mesothelial cell (HPMC) line HMrSV5 was co-incubated with gastric cancer cell supernatant (MKN45) and/or Astragalus memebranaceushas. Morphological changes in gastric cancer cells were observed under phase-contrast microscope. Quantitative cell damage was determined by MTT assay. Apoptosis was determined under transmission electron microscope and quantified by detecting acridine orange/ethidium bromide-stained (AO/EB) condensed nuclei under fluorescent microscope or by flow cytometry. Expressions of Bcl-2 and Bax were evaluated with immunostaining. RESULTS: Morphological changes and exfoliation occurred and naked areas appeared in culturedHMrSV5 cells 24 h after they were treated with gastric cancer cell supernatant. Cell supernatant from MKN45 gastric cancer cells induced apoptosis of HMrSV5 cells in a time-dependent manner. Obvious morphological changes were observed in cell apoptosis, such as condensation of chromatin, nuclear fragmentations and apoptotic bodies. Astragalus memebranaceus could partly suppress these changes and regulate the expressions of Bcl-2 and Bax in HMrSV5 cells. CONCLUSION:Gastric cancer cells induce apoptosis of HPMCs through the supernatant. Astragalus memebranaceushas inhibits this phenomenon and can be used an adjuvant chemothera-peutic agent in gastric cancer therapy.

show abstract

The Immunotherapeutic Effects of Astragalus Polysaccharide in Type 1 Diabetic Mice

Cited by 61 publications

References 29 publications

Insulin's impact on renal sodium transport and blood pressure in health, obesity, and diabetes

Insulin's impact on renal sodium transport and blood pressure in health, obesity, and diabetes

Chronic Effects of Berberine on Blood, Liver Glucolipid Metabolism and Liver PPARs Expression in Diabetic Hyperlipidemic Rats

Astragalus extract inhibits destruction of gastric cancer cells to mesothelial cells by anti-apoptosis

Contact Info

Product

Resources

About