ABSTRACT
Objective To investigate the effect of an ACE inhibitor ,perindopril ,on the expression of SR‐A in renal tubuloint‐erstitium of diabetic rats .Methods Diabetes was induced in male Sprague‐Dawley rats by injection with streptozotocin .The rats were then randomly divided into 3 groups:normal control group;untreated diabetes mellitus group and diabetes mellitus group trea‐ted with perindopril .After a 24‐week treatment ,tubulointerstitial injury index was assessed with Masson′s trichrome sections .The expression of SR‐A mRNA was detected by RT‐PCR and the expression of SR‐A protein in renal tubulointerstitium was detected by immunohistochemistry .Results The tubulointerstitial injury index ,the expression of SR‐A mRNA were significantly higher in the diabetes group than those in normal control group .Perindopril treatment not only attenuated the tubulointerstitial injury ,but also reduced the overexpression of SR‐A mRNA in diabetic rats .The expression of SR‐A protein was most obvious in renal tubulointer‐stitium in diabetic rats ,which was obviously attenuated by perindopril treatment(P<0 .05) .Conclusion The findings of the this study indicate that perindopril may have renoprotective effects on diabetic nephropathy via inhibiting the expression of SR‐A in re‐nal tubulointerstitium .
ABSTRACT
Objective To explore the effect of ACE-inhibitor perindopril on the expression of scavenger receptor A (SR-A) gene in the kidney of diabetic rats.Methods Diabetes were induced in male Sprague-Dawley rats by peritoneal injection with streptozotocin (60mg/kg).The rats were then random di vided into normal control group, diabetes group and ACEI treatment group [4mg/(kg·d) for 24 weeks].Blood glucose concentration and 24h urinary albumin excretion were determined.The renal morphological change was observed.Immunohistochemistry was used to analyze CD68 positive macrophages,and the Mrna of SR-A in renal tissue was detected by quantitative real-time PCR.Results Compared with normal control group,blood glucose concentration,24h urinary albumin excretion and the number of CD68 positive macrophages were significantly increased [(5.3 ± 0.6) mmol/L vs (26.7 ± 3.3) mmol/L;(2.7 ± 1.3) mg/24h vs (26.7 ± 1.8)mg/24h;(0.77 ±0.24)/gcs vs (2.55 ±0.46)/gcs;(6.13 ±0.50)/HPF vs (11.9 ±2.12)/HPF;P ＜0.05],and the expression of SR-A Mrna were significantly up-regulated in diabetes group [ (5.6 ± 1.2 vs 1.5 ±0.2),P ＜0.05].After intervention with ACE-inhibitor,the up-regulations of the above mentioned parameters,except blood glucose concentration,were all significantly inhibited [ (3.6 ±1.4)mg/24h;(1.03±0.37)/gcs;(8.28±1.19)/HPF;3.4±0.7;P ＜0.05].Conclusion ACE-inhibitor might have renoprotective effects of diabetic nephropathy,it probably was associated with inhibiting the expression of SR-A gene.
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Objective To investigate insulin sensitivity and beta cell function in female systemic lupus erythematosus (SLE) patients with different glucose tolerances. Methods Insulin sensitivity and beta cell function were compared between SLE patients and non-SLE subjects in the states of normal glucose tolerance (NGT), impaired glucose tolerance (IGT)and diabetes mellitus (DM) respectively.Furthermore, risk factors for insulin sensitivity and beta cell function in SLE patients were analysed by linear regression. Results In NGT state, insulin sensitivity and beta cell function of newly diagnosed SLE patients without glucocorticoids treatment were not significantly different from those of normal control group ( P ＜0. 05). Compared with newly diagnosed SLE patients without glucocorticoids treatment and normal control group, HOMA insulin resistance index (HOMA-IR) , In (HOMA-β), In (early phase insulin secretion index, EISI ) and In ( late phase insulin secretion index, LISI ) of SLE patients with glucocorticoids treatment were significantly higher( 1.91 ± 1.04 vs 0. 81 ±0. 75,0. 94 ±0. 27;5.05 ±0. 65 vs 4. 01 ±0. 63,4. 23 ±0.47;3. 14±0.81 vs 2.42 ±0.39,2.50±0.65;2.30 ±0.55 vs 1.62 ±0.57,1.56 ±0.43;P ＜0.05),while In ( Matsuda index, MI ) was significantly lower ( 4. 53 ± 0. 54 vs 5. 27 ± 0. 68,5. 18 ± 0. 38; P ＜0. 05). In IGT and DM state, HOMA-IR (2. 84 ± 1. 87 vs 1.82 ± 1.22, 3. 18 ±2. 29 vs 2. 94 ±2. 26) and In (HOMA-β) (5. 18 ±0. 93 vs 4. 06 ±0. 58, 3. 99 ± 1.04 vs 3.43 ±0. 83) were significantly higher in SLE patients with glucocorticoids treatment than those of non-SLE subjects ( P ＜ 0. 05 ) respectively. BMI and In (daily glucocorticords doses) were independent risk factors for insulin sensitivity, and age, the SLE disease activity index(SLEDAI) and In(daily glucocorticords doses) were related factors beta cell function.Conclusion In NGT, IGT and DM state,SLE female patients with glucocorticoids treatment have reduced insulin sensitivity and increased beta cell function, these changes are related to the use of glucocorticoids.
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Objective To research the effects of short-term intensive insulin treatment on regaining the sensitivity of sulfonylureas in diabetes patients. Methods Thirty patients from outpatient and emergency department,including 12 male and 18 female,who took regular-dose sulfonylureas but was high blood glucose level,were selected to suspend the sulfonylureas treatment and were given the BIAsp30 to control the blood glucose level for three months,then they were stopped the BIAsp30 and took the same sulfonylureas used before.Results The average fasting blood glucose(FBG) was(9.4?7.5)mmol/L and the average postprandial 2 h blood glucose(PG2h)(or random blood glucose) was(14.2?7.2)mmol/L in 3 months before stopping the sulfonylureas.The average FBG was(5.7?0.7)mmol/L and PG2h was(7.2?1.4)mmol/L at the beginning of the insulin getting the blood glucose under control.The average FBG was(6.0?0.8)mmol/L and PG2h was (7.8?1.2)mmol/L during the insulin treatment.The average FBG was(6.1?0.6)mmol/L and PG2 h was(7.7?1.3)mmol/L at the end of the insulin treatment.The average FBG was(6.5?0.5)mmol/L and PG2h was(8.1?(0.8))mmol/L when continuing the sulfonylureas treatment in one months.It increased significantly to compare the blood glucose before the treatment of insulin to that after the treatment of insulin(P