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Objective To detect the expression of miR-26a/b in the aorta and serum of mice so as to explore the role of miR-26a/b in vascular remodeling of hypertension.Methods C576L/BJ male mice were randomly divided into AngⅡ group and control group.Mini-osmotic pump was implanted subcutaneously into the back of mice, and the model of blood vessel remodeling in mice was established by continuous infusion of AngⅡ(2.0mg/kg·d).The mice in control group were injected with saline.Blood pressure was taken before the intervention and at 3, 5, 7, 10 and 14 days after the intervention.After 2 weeks, the mice were killed, the serum and aorta tissues were collected, and the expression of miR-26a/b was determined by RT-PCR.HE staining, Masson staining and immunohistochemistry were performed to observe changes in vascular morphology, fibrosis and protein expression.Results After the intervention, systolic blood pressure and diastolic blood pressure were significantly higher in AngⅡ group than in control group (P<0.05).HE staining showed that the vessel wall of AngⅡ group was thicker than that of control group.Masson staining showed more blue collagen deposition in the middle of aorta in AngⅡ group but no obvious collagen deposition in control group.RT-PCR showed that the expression of miRNA-26a/b in the serum and aorta of AngⅡ group was significantly lower than in control group (P<0.05).Immunohistochemistry indicated that the expressions of CTGF, collagen Ⅰ and collagen Ⅲ all increased after AngⅡ infusion (P<0.05).Conclusion MiR-26a/b, CTGF, collagen Ⅰ and collagen Ⅲ may be involved in AngⅡ-induced vascular remodeling in hypertension.MiR-26a/b may be a new therapeutic target of vascular remodeling in hypertension.
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1 1 patients with moderate or severe crowding in the anterior arch were treated with 4 premolar extraction.After canine distaliza-tion first approach,the teeth were aligned and leveled.The results of the study suggest that,with strict implementation of indication,this method may be a viable treatment for the moderate or severe crowding anterior.
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To investigate the expression of phosphorylated peroxisome proliferators-activated receptor γ (p-PPARγ) in the aging thoracic aorta of spontaneously hypertensive rat (SHR) and the inhibitory effect of rosiglitazone on the phosphorylation of PPARγ. Methods: 16, 32 and 64 week-old Wistar-Kyoto rats (WKY) and SHR were randomly and respectively divided into WKY, SHR and SHR+rosiglitazone group (9 in each group). The rats in SHR+rosiglitazone group were treated with rosiglitazone (5 mg/kg, intragastrically) for 56 d, whereas normal saline was applied in WKY and SHR groups. Systolic blood pressure (SBP) of rats was measured by tail cuff method. Histopathological damage of thoracic aorta was analyzed using Hematoxylin-Eosin (HE) staining. Immunohistochemical staining and western blot were performed to test the level of p-PPARγ protein in the thoracic aorta arising from each group. Results: The SBP in 16, 32 and 64 week-old SHR were significantly higher as compared with those in matched WKY rats (P<0.05, respectively). HE staining showed increased content of smooth muscle cell, wrinkled lining endothelium and increased thickness of internal elastic lamina in the thoracic aorta of SHR. Immunohistochemical staining and western blot indicated that the levels of p-PPARγ in the thoracic aorta arising from SHR were obviously higher than those in the thoracic aorta arising from WKY rats (P<0.05, respectively). Importantly, the high SBP, histopathological abnormalities of the thoracic aorta and elevated p-PPARγ expression were prominently abrogated by rosiglitazone treatment in SHR (P<0.05, respectively). Furthermore, the SBP, histopathological abnormalities of the thoracic aorta and p-PPARγexpression were positively correlated with age in SHR (P<0.05, respectively). Conclusions: The PPARγ phosphorylation was observed in the thoracic aorta of SHR and its expression was increased by the increase of age. Furthermore, rosiglitazone inhibited the PPARγ phosphorylation and suppressed vascular aging in SHR.
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Objective To investigate the effects of telmisartan on the expression of angiotensin converting enzyme2 (ACE2) mRNA in monocyte-derived macrophages of hypertensive patients companied with diabetes.Methods 62 essential hypertensive patients companied with diabetes were randomly divided into two groups:regular treatment group,and telmisartan group.Then the content of ACE and ACE2 in serum was detected by ELISA,and the expression of ACE mRNA and ACE2 mRNA in monocyte-derived macrophages of patients was detected by RT-PCR before and after having been treated.Results (1) After having been treated for 4 weeks and 12 weeks,the blood pressure of the patients in two groups were decreased significantly,Comparing with regular group,telmisartan group seemed to have more obvious therapeutic effect (P ＜ 0.05) ; (2) After having been treated for 12 weeks,glycosylated hemoglobin diseased in both group,but there was no significant difference between the two group (P ＞ 0.05) ; (3) In telmisartan group,the content of ACE2 in serum was increased after having been treated for 12 weeks than that in regular treatment group,[(23.9 ± 8.2) U/L vs (16.3 ± 8.9) U/L,P ＜ 0.05] ; and the expression of ACE2 mRNA in monocyte-derived macrophages in telmisartan group was obviously increased after 12 weeks comparing with regular treatment group (0.73 ±0.06 vs 0.51 ±0.04,P ＜0.01).Conclusion The role of telmisartan in decreasing blood pressure and it's advantage to the metabolism of glucose are partly related with the up-regulation of ACE2 mRNA.
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In order to investigate the impairment of mitochondrial membrane phospholipid localization and DNA(3867) (mtDNA(3867)) deletion and the correlation between cardiac and skeletal muscle cells in mice with viral myocarditis, 50 BALB/c mice were divided into two groups randomly. In experimental group (n=40), the mice were intraperitoneally injected with 0.1 mL Eagle liquid with CVB3(TCID50=10(8)), while in the control group (n=10), the mice were subjected to equal volume of Eagle liquid. The impairment of mitochondrial membrane phospholipid localization and mtDNA(3867) deletion rate of cardiac and skeletal muscle were detected separately at day 3, 11 and 24 after injection. The correlation of mitochondrial membrane phospholipid localization and mtDNA(3867) deletion rate between cardiac and skeletal muscle cells cells was analyzed using Spearman method. At the day 3 after injection, in both cardiac and skeletal muscle cells, mtDNA(3867) deletion rate was significantly higher in experimental group than in control group (P0.05). At day 11 after injection, the mtDNA(3867) deletion rate of both cells in experimental group was increased to the peak level (P0.05). At the day 24 after injection, the impairment of mitochondrial membrane phospholipid localization and mtDNA(3867) deletion of both cells showed a recovery tendency, but still severer than those at the day 3 after injection (P<0.05). The impairment of mitochondrial membrane phospholipid localization and mtDNA(3867) deletion were consistent and synchronistic between cardiac and skeletal muscle cells, and showed good correlations (P<0.05). The impairment of mitochondria plays an important role in the pathogenesis of viral myocarditis, and the skeletal muscle cells might act as a peripheral "window" to reflect the mitochondrial damage of cardiac myocytes.
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In order to investigate the impairment of mitochondrial membrane phospholipid localization and DNA3867 (mtDNA3867) deletion and the correlation between cardiac and skeletal muscle cells in mice with viral myocarditis, 50 BALB/c mice were divided into two groups randomly. In experimental group (n=40), the mice were intraperitoneally injected with 0.1 mL Eagle liquid with CVB3 (TCID50=108), while in the control group (n=10), the mice were subjected to equal volume of Eagle liquid. The impairment of mitochondrial membrane phospholipid localization and mtDNA3867 deletion rate of cardiac and skeletal muscle were detected separately at day 3, 11 and 24 after injection. The correlation of mitochondrial membrane phospholipid localization and mtDNA3867 deletion rate between cardiac and skeletal muscle cells cells was analyzed using Spearman method. At the day 3 after injection, in both cardiac and skeletal muscle cells, mtDNA3867 deletion rate was significantly higher in experimental group than in control group (P＜0.05), but the localization of mitochondrial membrane phospholipid showed no difference between two groups (P＞0.05). At day 11 after injection, the mtDNA3867 deletion rate of both cells in experimental group was increased to the peak level (P＜0.05), and the impairment of mitochondrial membrane phospholipid localization of both cells also increased markedly in experimental group as compared with control group (P＞0.05). At the day 24 after injection, the impairment of mitochondrial membrane phospholipid localization and mtDNA3867 deletion of both cells showed a recovery tendency, but still severer than those at the day 3 after injection (P＜0.05). The impairment of mitochondrial membrane phospholipid localization and mtDNA3867 deletion were consistent and synchronistic between cardiac and skeletal muscle cells, and showed good correlations (P＜0.05). The impairment of mitochondria plays an important role in the pathogenesis of viral myocardifis, and the skeletal muscle cells might act as a peripheral "window" to reflect the mitochondrial damage of cardiac myocytes.
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OBJECTIVE: To observe the promoting effect of arnebia root oils on expression of basic fibroblast growth factor (bFGF) in skin wound of rabbits and the histomorphological changes in the wound surface, and to discuss its mechanism. METHODS: Bilateral round skin wounds were made on the back of 15 rabbits. The three wounds on one side of the back of each rabbit were treated with arnebia root oils, while the three wounds on the other side were treated with vaseline in order to promote the wound healing. The histomorphology and ultrastructure under electron microscopy of the wounds, and the rate of wound healing were examined at different time. Western blotting assay was used to detect the expression of bFGF in the wound surface. RESULTS: The healing rate of the arnebia root oils-treated wounds was evidently higher than that of the vaseline-treated wounds (P<0.05). The quantities of fibroblast, collagen and capillary in the arnebia root oils-treated wounds were much more than those in the vaseline-treated wounds, and the expression of endogenous bFGF in the arnebia root oils-treated wounds was enhanced obviously as compared with that in the vaseline-treated wounds in different period of wound healing. There existed a parallel correlation between the expression level of bFGF and the rate of wound healing. CONCLUSION: The promoting effect of arnebia root oils on wound healing may be related to increasing the expression level of basic fibroblast growth factor in the skin wound.
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<p><b>OBJECTIVE</b>To explore the molecular biological mechanism of Arnebia Root oil (AO) in promoting the recovery of surface of wound by observing basic fibroblast growth factor (bFGF) mRNA expression in the wound tissue and healing rate of the wound.</p><p><b>METHODS</b>Patients in the observed group with their wound treated by AO and those in the control group treated by petrolatum gauze. The wound surface healing rate was estimated and bFGF mRNA expression was observed by RT-PCR.</p><p><b>RESULTS</b>Endogenous bFGF mRNA expression existed in the wound surface of both groups, but its level in the observed group at any time point was obviously higher than that in the control group respectively, with significant difference in comparison of the gray density between the two groups (P < 0.05). The wound surface healing rate kept abreast with bFGF mRNA expression in wound tissues, so it was significantly higher in the observed group than that in the control group (P < 0.05). GAPDH gene, which was taken as a parameter for internal reference, expressed with a certain amount unchanged in different periods of healing (P > 0.05 ).</p><p><b>CONCLUSION</b>AO shows obviously promotive action on bFGF, an important regulatory factor on wound healing, it might complete the recovery process by stimulating the increase of bFGF.</p>
Subject(s)
Adolescent , Adult , Female , Humans , Male , Middle Aged , Boraginaceae , Chemistry , Drugs, Chinese Herbal , Fibroblast Growth Factor 2 , Genetics , Phytotherapy , Plant Oils , Plant Roots , Chemistry , RNA, Messenger , Genetics , Wound Healing , Wounds and Injuries , Drug Therapy , MetabolismABSTRACT
Objective To investigate the effect of all-trans retinoic acid(atRA) on the urinary TGF?_1 excretion and glomerular lesion of diabetic rats at early stage.Methods SD rats were randomly assigned into 3 groups: atRA treated group,diabetic control group and normal control group.Streptozotocin(STZ)-induced early diabetic male SD rat were used.The atRA treated group were treated with daily subcutaneous injections atRA of 10mg/kg for 7 days(n=6),and then the excretion of urinary protein and TGF?_1 and NO level of plasma,urine and renal tissue were measured,and pathological changes of their kidneys were observed.Results The diabetic control rats showed increased urinary excretion of protein and TGF?_1 and NO level of plasma,urine and renal tissue and deposit of glomerular matrix,while atRA prevented these changes.Conclusion AtRA can prevent the development of diabetic nephropathy,which is relevant with the inhibition of secretion of TGF?_1 and NO.
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AIM: To elucidate the role of mitochondrial DNA (mtDNA) deletion in the pathogenesis of viral myocarditis in mice. METHODS: 50 BALB/c mice were divided into two groups randomly. 40 were experimental group, each of them was injected 0.1 mL Eagle liquids with CVB_3 (TCID_ 50=108) intraperitoneally. Another 10 mice were given equal volume Eagle liquids as control group. Cardiac functions in vivo and mtDNA 3867 deletion rate in myocytes were detected separately at the day 3, 11 and 24 after injection. The correlation of mtDNA 3867 deletion rate to cardiac functions was analyzed using Spearman method. RESULTS: At the day 3 after injection, mtDNA 3867 deletion rate in experimental group was 8.3 times higher than that in control group [(0.01970?0.00118)% vs (0.00211?0.00032)%,P
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Objective To study the effect of Benazepril on the renal connective tissue growth factor(CTGF) expression and interstitial fibrosis in unilateral ureteral obstruction(UUO) rats and to illuminate the possible mechanisms.Methods 24 Sprague-Dawley rats were randomly divided into Sham-operated,control and Benazepril groups.From the day before operation,the rats were under intragastric administration of Benazepril 10mg/(kg?d) in Benazepril group,and sodium chloride in tales doses in Sham and control groups.On the 14~(th) day after operation,the obstructed kidney was taken out to be measured by HE,Masson,and immunohistochemistry staining for TGF-?_1,CTGF,?-SMA and ColⅢ.Results The score of renal interstitial lesion and fibrosis index in Benazenpril were significantly lower than those in the control group(P
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Objective To investigate the effect of at-RA in macrophage accumulation in tubulointerstitium of rats with renal tubulointerstitial fibrosis.Methods Unilateral ureteral obstructive(UUO) rat animal models were used for the study.40 SD rats were randomly divided into 5 groups: sham group,UUO group,benazepril group,low-dose at-RA groups and high-dose at-RA groups.The rats were under intragastric administration by benazepril(10mg/(kg?d)) in benazepril group,and by(at-RA)(10mg/(kg?d)) in low-dose at-RA group and 20mg/(kg?d) in high-dose at-RA group and by sodium chloride in tales doses in sham group and UUO group from the day before the operation to 14 day after operation.Immunohistochemistry staining of CD68 and Col Ⅲ was used to define the macrophage accumulation and expression of interstitial Col Ⅲ.The degree of tubulointerstitial damage was scored by HE and Masson staining.Results Tubulointerstitial macrophage infiltration were all significantly reduced by(at-RA) or benazepril treatment.They also improved the histological changes of UUO rats and inhibited interstitial colⅢ deposition.Conclusion Reduction of interstitial macrophage infiltration may be an important event by which(at-RA) or benazepril prevents renal injury caused by UUO.
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Objective To investigate the protective function of oxymatrine on the renal intestitial fibrosis in rats.Methods Forty male Sprague Dawley rats were randomly divided into 5 groups: sham group,model group,Lotensin group,large-dose oxymatrine group,and small-dose oxymatrine group.The models were established by unilateral ureteral obstruction(UUO) of the left side.On the 14~(th) day after operation,the obstructed kidney was taken out.Then,HE,Massion,and immunohistochemistry staining of transforming growth factor-?_(1)(TGF-?_(1)),(?-smooth) muscle acting(?-SMA) and collagen Ⅲ were conducted.After that,semiquantitative analysis was performed.Results After oxymatrine,treatment,the expressions of ?-SMA,TGF-?_(1) and ColⅢ of the obstructed kidney in the treatment group were significantly lower than those in the model group(P0.05).Conclusion Oxymatrine may reduce the expression of cytokines such as TGF-?_(1),then the activation of cell producing ECM and then the sendimentation of ECM,thus preventing renal interstitial fibrosis.