Effects of Cordyceps sinensis on the Expressions of NF-κB and TGF-ß1 in Myocardium of Diabetic Rats.

Objective. To investigate the effect of Cordyceps sinensis (CS) on the expressions of NF-κB and TGF-ß1 in myocardium of streptozotocin-induced diabetic rats. Methods. A total of 53 healthy male SD rats, mice age of 8 weeks and weight of 220 ± 20 g, were randomly divided into five groups by randomized block design: normal control group (n = 10), diabetic group (n = 10), low dose of CS group (n = 12; CS 0.6 g·kg(-1)·d(-1)), middle dose of CS group (n = 11; CS 2.5 g·kg(-1)·d(-1)), and high dose of CS group (n = 10; CS 5 g·kg(-1)·d(-1)). The diabetic models with tail intravenous injection by streptozotocin (45 mg·kg(-1)). Diabetic rats were sacrificed after 8 weeks; the expressions of NF-κB and TGF-ß1 proteins and mRNA in the cardiac muscle were determined by using immunohistochemistry staining and reverse transcription polymerase chain reaction (RT-PCR) method. The data were analyzed using one factor analysis of variance. Result. The expressions of NF-κB and TGF-ß1 proteins and mRNA in the cardiac muscle of diabetic rats were significantly raised (P < 0.05), which could be decreased by CS (P < 0.05). Conclusions. The changes on the expressions of NF-κB and TGF-ß1 in myocardium may be involved in the occurrence of diabetic cardiomyopathy (DC). CS may play its role on myocardial protection by regulating the expressions of NF-κB and TGF-ß1 in myocardium.

1,25(OH)2D3-mediated amelioration of aortic injury in streptozotocin-induced diabetic rats.

In this study, a single tail vein injection of streptozotocin (STZ)-induced rat model was employed to study the effects of 1,25(OH)2D3 supplementation, the active form of vitamin D, on diabetes-induced aortic injury. Aortas from different groups were assessed for histopathology, toll-like receptor 4 (TLR4), myeloid differentiation primary response gene 88 (MyD88), and nuclear factor-kappa B (NF-κB) p65 expression by hematoxylin and eosin staining, immunohistochemistry staining, reverse transcription polymerase chain reaction, and Western blot analysis. High-dose 1,25(OH)2D3 (0.3 µg/kg/day) significantly prevented diabetes-induced aortic pathological changes and collagen deposition and decreased the expression of TLR4, MyD88, and NF-κB at both mRNA and protein levels in the aorta of STZ-induced diabetic rats (P < 0.01). In vitro studies in A7r5 cells (a rat embryonic thoracic aortic smooth muscle cell line) showed that high-dose glucose (25 mmol/L) enhanced TLR4 expression at both mRNA and protein levels by fourfold and twofold, respectively, at 24 h, which were significantly diminished by 1,25(OH)2D3 (1 × 10(-7) mol/L) by 50 and 36 %, respectively. Similar effects of high-dose 1,25(OH)2D3 on the expression of MyD88 were observed. Our results indicate that vitamin D has protective effects on diabetes-induced aortic injury and attenuates the expressions of TLR4, MyD88, and NF-κB in diabetic rats.

[Clinical analysis of drug-induced Pseudo-Bartter's syndrome: a report of five cases].

OBJECTIVE: To summarize the clinical characteristics and outcomes of Pseudo-Bartter's syndrome and explore its pathogenesis. METHODS: The clinical data of 5 cases of Pseudo-Bartter's syndrome at our ward from May 2008 to December 2010 was analyzed retrospectively. RESULTS: All patients were female. Long-term regimen of purgative or diuretics was prescribed. The clinical features included normotension, hypokalemic alkalosis and activation of renin-angiotensin-aldosterone. The pathological results of 3 cases of kidney biopsy showed the hyperplasia of juxtaglomerular apparatus, thickness of arteriole, infiltration of lymphocytes and monocytes and degeneration of renal tubule. Upon a definitive diagnosis, purgative or diuretics was discontinued and supplement therapy of potassium chloride initiated. The results of laboratory tests reverted to normal ranges within 4 weeks. CONCLUSION: Purgative or diuretics should be prescribed appropriately to avoid the occurrence of Pseudo-Bartter's syndrome.

[Clinical analysis of 6 cases of Bartter syndrome].

OBJECTIVE: To summarize the clinical characteristics of Bartter syndrome and investigate its pathogenesis. METHODS: The clinical data of 6 cases of Bartter syndrome at our hospital from November 2006 to May 2010 were analyzed retrospectively. RESULTS: The onset age of Bartter syndrome was 13-35 years old. The main symptoms included weakness (6/6), paralysis (1/6), numbness (5/6) and tetany (4/6). All patients had normal blood pressure. The biochemical tests showed persistent hypokalemia, metabolic alkalosis (6/6) and hyperreninemia. The pathological examination of deltoid muscle biopsy showed the swelling, degeneration and necrosis of myocytes and the deposition of immunocomplex in myolemma. And the pathological examination of renal biopsy showed the hyperplasia of juxtaglomerular apparatus (5/6) and the deposition of immunocomplex. All symptoms were relieved after a therapy of potassium supplementation or a combination of indomethacin, spironolactone and immunosuppressant. CONCLUSION: When such clinical features as weakness, paralysis, tetany, hypokalemic alkalosis and normotension are encountered, Bartter syndrome should be suspected. Serum electrolytes, blood gas analysis and activation of the renin-angiotensin-aldosterone system should be examined for a definite diagnosis. The treatment of choice includes potassium and magnesium supplementation or in combination with prostaglandin synthetase inhibitor, aldosterone antagonist and immunosuppressant. Immunologic mechanism may participate in the course of Bartter syndrome.

[Effects of supplementation of different kinds of iodine on the antioxidative ability of retina in iodine deficient rats].

OBJECTIVE: To study the effects of iodine supplementation (in different kinds and doses) on the antioxidative ability of retina in iodine deficient rats. METHODS: One hundred and twenty eight iodine deficient Wistar rats were randomly divided into four groups, normal dose of iodate, normal dose of iodide, high dose of iodate and high dose of iodide. Concentration of serum thyroid hormones, including total TT(3) and total TT(4), were estimated by radioimmunoassay. GSH-Px, SOD, TAOC activities and MDA content in the retina were determined using biochemical methods in the 22nd week of iodine supplementation. RESULTS: Statistical analysis showed that a significant difference in TT(3) level of serum was observed between animals treated with different doses. Serum TT(3) level in the groups treated with high doses was significantly higher than those with normal doses. However, no statistical difference could be detected at TT(4) level between animals treated with different doses. Different kind of iodine did not affect the level of thyroid hormones. Statistical analysis showed that a difference in SOD activity of retina was observed between animals treated with different doses. SOD activity in the groups with normal doses was significantly higher than that in groups with larger doses. Retina TAOC activity was significantly higher in groups treated with iodide than that in groups of iodate. Although there was no statistical difference in GSH-Px activity between different groups, it showed the same tendency as the SOD and TAOC activities, i.e. GSH-Px activity in the groups of normal doses was higher than that in the groups of high doses. GSH-Px activity in groups of iodide was higher than that in the groups of iodate. There was no significant difference in MDA content among these four groups. CONCLUSIONS: Different iodine and doses have certain effects on the antioxidative ability of retina in iodine deficient rat. The rats supplemented potassium iodide at normal dose showed higher antioxidative ability of the retina than those of the others.