Oral magnesium administration prevents vascular complications in STZ-diabetic rats

Soltani, Nepton; Keshavarz, Mansoor; Sohanaki, Hamid; Dehpour, Ahmad Reza; Asl, Saleh Zahedi

doi:10.1016/j.lfs.2004.07.027

Cited by 23 publications

(24 citation statements)

References 15 publications

(21 reference statements)

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“…In previous work, Soltani et al, showed that a significant reduction in Mg level in acute diabetic groups [32]. These discrepancy may be due to the dose of STZ and the model of diabetes induction.…”

Section: Discussionmentioning

confidence: 99%

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Protective effect of magnesium on renal function in STZ-induced diabetic rats

Parvizi

Parviz

Tavangar

et al. 2014

J Diabetes Metab Disord

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BackgroundDiabetic nephropathy is a serious complication of T1D (type one diabetes mellitus). Persistent hyperglycemia and subsequent hypomagnesemia is believed to develop kidney damage by activation of oxidative stress. We conducted this study to investigate the renoprotective effect of magnesium sulfate (MgSO4) on renal histopathology and oxidative stress in diabetic rats.MethodsThe study included 70 male rats. The animals were divided into seven groups: control (CRL), control receiving MgSO4 (CRL + Mg1 & CRL + Mg8), diabetic (DM1 & DM8) and diabetic receiving MgSO4 (DM + Mg1 & DM + Mg8). Rats were given 20 mg/kg (i.p) Streptozocin (STZ) for 5 consecutive days in (MLD) multiple low doses to induce T1D. At day 10 treatment groups were received MgSO4 (10 g/l) in drinking water, for 1 or 8 weeks. The blood glucose, BUN and creatinine levels were measured. Renal tissue levels of malondialdehyde (MDA) were measured by thiobarbituric acid (TBA) method to evaluate the oxidative stress. Renal histopathology was done using H & E staining method.ResultsTreatment with MgSO4 significantly decreased the blood glucose in DM + Mg1 and DM + Mg8 groups as compared with DM1 and DM8. Magnesium treatment also decreased serum BUN and tissue level of MDA significantly in both short and long term treatment. The body weight loss and kidney weight to body weight ratio was improved by MgSO4. Histological results showed there were no differences between DM and DM + Mg groups.ConclusionOur findings showed that diabetic nephropathy is associated with high blood glucose level and oxidative stress (significant increase in MDA level). The renal dysfunction and oxidative stress can be improved by magnesium sulfate administration. It is suggested that protection against development of diabetic nephropathy by MgSO4 treatment involves changes in the blood glucose and oxidative stress.

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Section: Discussionmentioning

confidence: 99%

“…It could improve some of diabetic complications such as hypertension [19,32], thermal hyperalgesia and structure of pancreatic islets [20,33]. Also MgSO 4 improves function of endothelium and restores hemodynamic and tubular function in postischemic rats [34].…”

Section: Discussionmentioning

confidence: 99%

Protective effect of magnesium on renal function in STZ-induced diabetic rats

Parvizi

Parviz

Tavangar

et al. 2014

J Diabetes Metab Disord

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“…Recent studies have shown that in diabetic rats, Mg deficiency is induced by Streptozocin (STZ) (11-15). Mg as an essential ion plays important roles in physiological processes.…”

Section: Introductionmentioning

confidence: 99%

“…Administration of Mg supplementation reduces the oxidative stress in Alloxan-induced diabetic rats (18). Recent studies have shown that oral administration of Mg compounds may be able to attenuate hypomagnesaemia (11, 13, 15), hyperglycemia (13, 14), and thermal hyperalgesia (15) in diabetic rats; and also prevent vascular complication induced by the diabetic state (11). Studies have indicated that uncontrolled STZ-induced diabetes in rats could protect renal tissue against CP-induced damage (19-22).…”

Section: Introductionmentioning

confidence: 99%

Effect of Oral Administration of Magnesium on Cisplatin-Induced Nephrotoxicity in Normal and Streptozocin-Induced Diabetic Rats

et al. 2013

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BackgroundCisplatin (CP) therapy as the most common potent chemotherapeutic process is accompanied by nephrotoxicity. The diabetic state may protect rat kidney against this toxicity, and magnesium (Mg) on the other hand may reduce the glucose level in diabetic animals.ObjectivesCurrent study was planned to investigate the effect of oral administration of magnesium supplementation on CP-induced nephrotoxicity in normal and Streptozocin (STZ)-induced diabetic rats.Materials and MethodsMale Wistar rats were divided into seven groups and underwent two experiment protocols. As protocol 1, group 1 was considered as the sham group. Group 2 (CP group) received CP (2 mg/kg/d) for five consecutive days. Group 3 (CP + Mg group) received magnesium sulphate (MgSO4, 10 g/L added to the drinking water) for 10 days and then treated with CP from sixth day. As protocol 2, animals received a single dose of STZ (65 mg/kg i.p.). Three days after diabetes induction, animals were divided into four groups; Groups 4 (D group), 5 (D + CP group), and 7 (D + Mg + CP group) followed the same manner as groups 1 to 3, respectively; and group 6 (D + Mg group) was treated with MgSO4 alone for 10 days. Finally, blood samples were obtained, and all animals were killed for kidney tissue investigation.ResultsCP administration in normoglycemic rats significantly elevated the serum levels of blood urea nitrogen (BUN) and creatinine (Cr) (P < 0.05). However, coadministration of CP and Mg statistically increased the serum levels of BUN and Cr in both normoglycemic and diabetic animals when compared to the rats treated with CP alone (P < 0.05), while the serum level of Mg was significantly increased in nondiabetic groups (P < 0.05). No significant changes were observed in serum and kidney levels of nitrite; as well as the testis weight between all normoglycemic groups, whereas Mg decreased kidney levels of nitrite in diabetic groups when accompanied by CP (P < 0.05). The kidney and serum levels of malondialdehyde (MDA) enhanced significantly in nondiabetic rats treated with Mg and CP (P < 0.05). Kidney tissue damage score (KTDS), kidney weight, and body weight loss were significantly different among normoglycemic groups (P < 0.05), and Mg promoted the KTDS in diabetic animals treated with CP.ConclusionsOral Mg supplementation did not protect the CP induced nephrotoxicity in diabetic rats.

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“…Our previous studies (Soltani et al 2005a), showed that plasma magnesium level in diabetic rats was significantly lower than non diabetic ones and administration of Mg 2+ could prevent diabetes vascular complications. According to our previous studies (Soltani et al 2005a,b,c), Mg 2+ supplementation produced vasorelaxation in both diabetic and non-diabetic mesenteric vascular beds.…”

Section: Discussionmentioning

confidence: 95%

Mg2+-induced adenosine-receptor mediated relaxations in mesenteric vascular beds of diabetic rats

Tavasoli¹,

Soltani²,

Keshavarz³

et al. 2012

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Abstract.Our previous studies showed that the magnesium Mg 2+ -induced relaxations were completely dependent on concentration of nitric oxide (NO) in non-diabetic rat mesenteric vascular beds, in diabetic rats other mechanisms may be involved. The present study was designed to determine the role of adenosine receptor in Mg 2+ -induced relaxation in streptozotocin (STZ)-induced diabetic rats vessels. Diabetes was induced by the intravenous injection of 60 mg/kg STZ. Eight weeks after diabetes induction, superior mesenteric arteries were isolated and perfused according to the McGregor method. Prepared vascular beds were constricted with phenylephrine to induce 70-75% of maximal constriction (0.001 M). Mg 2+ at concentrations of 10 -4 to 10 -1 M were added into the medium and perfusion pressure was recorded. Theophylline (1 mM), and 3,7-dimethyl-1-propargylxanthine (0.01 μM) were added into medium 20 min before phenylephrine administration. In the presence of theophylline, vasorelaxation induced by high dose of Mg 2+ (from 0.03 to 0.1 M) was totally suppressed. In presence of N(ω)-nitro-L-arginine methyl ester (L-NAME), the response of Mg 2+ was completely inhibited at low dose of Mg 2+ . But, Mg 2+ -induced relaxation in the presence of adenosine A2a receptor blocker was significantly suppressed in high dose of Mg 2+ . Mg 2+ -induced relaxation in the presence of an A2a receptor blocker was not suppressed either by denudation of endothelium or presence of L-NAME. From the results of this study it may be concluded that Mg 2+ -induced relaxation at high concentrations is mediated by adenosine A2a receptors, but at low concentrations Mg 2+ -induced relaxation is dependent on NO.

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Oral magnesium administration prevents vascular complications in STZ-diabetic rats

Cited by 23 publications

References 15 publications

Protective effect of magnesium on renal function in STZ-induced diabetic rats

Protective effect of magnesium on renal function in STZ-induced diabetic rats

Effect of Oral Administration of Magnesium on Cisplatin-Induced Nephrotoxicity in Normal and Streptozocin-Induced Diabetic Rats

Mg2+-induced adenosine-receptor mediated relaxations in mesenteric vascular beds of diabetic rats

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