scholarly journals Benidipine Protects Kidney through Inhibiting ROCK1 Activity and Reducing the Epithelium-Mesenchymal Transdifferentiation in Type 1 Diabetic Rats

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Ganlin Wu ◽  
Meirong Xu ◽  
Kui Xu ◽  
Yilan Hu
Keyword(s):  
Interstitial Fibrosis ◽  
Rho Kinase ◽  
Inflammatory Cells ◽  
Cell Number ◽  
Diabetic Rats ◽  
Renal Tubular Epithelium ◽  
Group D ◽  
E Cadherin

We investigated the protective effect of benidipine, by testing the changes of the activity of Rho kinase and transdifferentiation of renal tubular epithelium cellsin vivo. Wistar rats were randomly divided into two groups: normal (N) and diabetes. STZ were used to make the rats type 1 diabetic and were randomly assigned as diabetes without treatment (D), diabetes treated with benidipine (B), and diabetes treated with fasudil (F) and treated for 3 months. Immunohistochemistry and western blotting were for protein expressions of ROCK1,α-SMA, and E-cadherin and real-time PCR for the mRNA quantification of ROCK1. Compared with N group, D group had significant proliferation of glomerular mesangial matrix, increased cell number, thickened basement membrane, widely infiltrated by inflammatory cells and fibrosis in the renal interstitial, and dilated tubular. Those presentations in F and B groups were milder. Compared with N group, D group showed elevated MYPT1 phosphorylation, increased expression of ROCK1,α-SMA protein, and ROCK1 mRNA and decreased expression of E-cadherin protein. B group showed attenuated MYPT1 phosphorylation, decreased ROCK1,α-SMA protein, and ROCK1 mRNA expression and increased expression of E-cadherin protein. In conclusion, benidipine reduces the epithelium-mesenchymal transdifferentiation and renal interstitial fibrosis in diabetic kidney by inhibiting ROCK1 activity.

scholarly journals The Effects of Lycopene and Insulin on Histological Changes and the Expression Level of Bcl-2 Family Genes in the Hippocampus of Streptozotocin-Induced Diabetic Rats

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Masoume Soleymaninejad ◽  
Seyed Gholamali Joursaraei ◽  
Farideh Feizi ◽  
Iraj Jafari Anarkooli
Keyword(s):  
Cell Death ◽  
Wistar Rats ◽  
Diabetic Rats ◽  
Expression Level ◽  
Histological Changes ◽  
Group D

The aim of this study was to evaluate the effects of antioxidants lycopene and insulin on histological changes and expression of Bcl-2 family genes in the hippocampus of streptozotocin-induced type 1 diabetic rats. Forty-eight Wistar rats were divided into six groups of control (C), control treated with lycopene (CL), diabetic (D), diabetic treated with insulin (DI), diabetic treated with lycopene (DL), and diabetic treated with insulin and lycopene (DIL). Diabetes was induced by an injection of streptozotocin (60 mg/kg, IP), lycopene (4 mg/kg/day) was given to the lycopene treated groups as gavages, and insulin (Sc, 1-2 U/kg/day) was injected to the groups treated with insulin. The number of hippocampus neurons undergoing cell death in group D had significant differences with groups C and DIL (p<0.001). Furthermore, insulin and lycopene alone or together reduced the expression of Bax, but increased Bcl-2 and Bcl-xL levels in DI, DL, and DIL rats, especially when compared to group D (p<0.001). The ratios of Bax/Bcl-2 and Bax/Bcl-xL in DI, DL, and DIL rats were also reduced (p<0.001). Our results indicate that treatment with insulin and/or lycopene contribute to the prevention of cell death by reducing the expression of proapoptotic genes and increasing the expression of antiapoptotic genes in the hippocampus.

scholarly journals Exercise training normalizes impaired NOS-dependent responses of cerebral arterioles in type 1 diabetic rats

2011 ◽  
Vol 300 (3) ◽  
pp. H1013-H1020 ◽  
Author(s):  
William G. Mayhan ◽  
Denise M. Arrick ◽  
Kaushik P. Patel ◽  
Hong Sun
Keyword(s):  
Exercise Training ◽  
Brain Tissue ◽  
Diabetic Rats ◽  
Protein Levels ◽  
Pial Arterioles ◽  
Cerebral Arterioles ◽  
Oxide Synthase ◽  
Enos Protein

Our goal was to examine whether exercise training (ExT) could normalize impaired nitric oxide synthase (NOS)-dependent dilation of cerebral (pial) arterioles during type 1 diabetes (T1D). We measured the in vivo diameter of pial arterioles in sedentary and exercised nondiabetic and diabetic rats in response to an endothelial NOS (eNOS)-dependent (ADP), an neuronal NOS (nNOS)-dependent [ N-methyl-d-aspartate (NMDA)], and a NOS-independent (nitroglycerin) agonist. In addition, we measured superoxide anion levels in brain tissue under basal conditions in sedentary and exercised nondiabetic and diabetic rats. Furthermore, we used Western blot analysis to determine eNOS and nNOS protein levels in cerebral vessels/brain tissue in sedentary and exercised nondiabetic and diabetic rats. We found that ADP and NMDA produced a dilation of pial arterioles that was similar in sedentary and exercised nondiabetic rats. In contrast, ADP and NMDA produced only minimal vasodilation in sedentary diabetic rats. ExT restored impaired ADP- and NMDA-induced vasodilation observed in diabetic rats to that observed in nondiabetics. Nitroglycerin produced a dilation of pial arterioles that was similar in sedentary and exercised nondiabetic and diabetic rats. Superoxide levels in cortex tissue were similar in sedentary and exercised nondiabetic rats, were increased in sedentary diabetic rats, and were normalized by ExT in diabetic rats. Finally, we found that eNOS protein was increased in diabetic rats and further increased by ExT and that nNOS protein was not influenced by T1D but was increased by ExT. We conclude that ExT can alleviate impaired eNOS- and nNOS-dependent responses of pial arterioles during T1D.

scholarly journals Is Autologous or Heterologous Pericardium Better for Valvuloplasty? A Comparative Study of Calcification Propensity

2015 ◽  
Vol 42 (3) ◽  
pp. 202-208 ◽  
Author(s):  
Wen-Jian Jiang ◽  
Yong-Chao Cui ◽  
Jin-Hua Li ◽  
Xiu-Hui Zhang ◽  
Huan-Huan Ding ◽  
...  
Keyword(s):  
Calcium Content ◽  
Inflammatory Cells ◽  
Autologous Pericardium ◽  
Group A ◽  
Group B ◽  
Pericardial Calcification ◽  
Group D ◽  
Collagenous Fibers

Pericardial calcification is detrimental to the long-term durability of valvuloplasty. However, whether calcification susceptibility differs between heterologous and autologous pericardium is unclear. In this study, we compared the progression of calcification in vivo between autologous and heterologous pericardium. We randomly divided 28 rabbits into 4 equal groups. Resected rabbit pericardium served as autologous pericardium, and commercial bovine pericardium served as heterologous pericardium. We subcutaneously embedded one of each pericardial patch in the abdominal walls of 21 of the rabbits. The 7 control rabbits (group A) received no implants. The embedded samples were removed at 2 months in group B, at 4 months in group C, and at 6 months in group D. Each collected sample was divided into 2 parts, one for calcium-content measurement by means of atomic-absorption spectroscopy, and one for morphologic and histopathologic examinations. When compared with the autologous pericardium, calcium levels in the heterologous pericardium were higher in groups B, C, and D (P &lt;0.0001, P &lt;0.0002, and P &lt;0.0006, respectively). As embedding time increased, calcium levels in the heterologous pericardium increased faster than those in the autologous, especially in group D. Disorganized arrangements of collagenous fibers, marked calculus, and ossification were seen in the heterologous pericardium. Inflammatory cells—mainly lymphocytes and small numbers of macrophages—infiltrated the heterologous pericardium. The autologous pericardium showed a stronger ability to resist calcification. Our results indicate that autologous pericardium might be a relatively better choice for valvuloplasty.

scholarly journals Cardiac Lymphatic Dysfunction Causes Drug-Eluting Stent–Induced Coronary Hyperconstricting Responses in Pigs In Vivo

2019 ◽  
Vol 39 (4) ◽  
pp. 741-753 ◽  
Author(s):  
Hirokazu Amamizu ◽  
Yasuharu Matsumoto ◽  
Susumu Morosawa ◽  
Kazuma Ohyama ◽  
Hironori Uzuka ◽  
...  
Keyword(s):  
Experimental Studies ◽  
Lymphatic Vessels ◽  
Rho Kinase ◽  
Inflammatory Cells ◽  
Bare Metal Stent ◽  
Drug Eluting Stent ◽  
Kinase Activation ◽  
Coronary Vasomotion ◽  
Drug Eluting

Objective— We have previously demonstrated that coronary adventitial inflammation plays important roles in the pathogenesis of coronary vasomotion abnormalities, including drug-eluting stent (DES)–induced coronary hyperconstricting responses. Importantly, the adventitia also harbors lymphatic vessels, which may prevent inflammation by transporting extravasated fluid and inflammatory cells. We thus aimed to examine the roles of coronary adventitial lymphatic vessels in the pathogenesis of DES-induced coronary hyperconstricting responses in a porcine model in vivo. Approach and Results— We performed 2 experimental studies. In protocol 1, 15 pigs were divided into 3 groups with or without DES and with bare metal stent. Nonstented sites 20 mm apart from stent implantation also were examined. In the protocol 2, 12 pigs were divided into 2 groups with or without lymphatic vessels ligation followed by DES implantation at 2 weeks later (n=6 each). We performed coronary angiography 4 weeks after DES implantation, followed by immunohistological analysis. In protocol 1, the number and the caliber of lymphatic vessels were greater at only the DES edges after 4 more weeks. In protocol 2, coronary hyperconstricting responses were further enhanced in the lymphatic vessels ligation group associated with adventitial inflammation, Rho-kinase activation, and less adventitial lymphatic vessels formation. Importantly, there were significant correlations among these inflammation-related changes and enhanced coronary vasoconstricting responses. Conclusions— These results provide evidence that cardiac lymphatic vessel dysfunction plays important roles in the pathogenesis of coronary vasoconstrictive responses in pigs in vivo.

Nrf2 Improves Airway Goblet Cell Metaplasia in Chronic Obstructive Pulmonary Disease (COPD) and Its Mechanism

2022 ◽  
Vol 12 (4) ◽  
pp. 739-746
Author(s):  
Zhihong Qiu ◽  
Li Yan ◽  
Juan Xu ◽  
Xiaojun Qian
Keyword(s):  
Protein Expression ◽  
Goblet Cell ◽  
Inflammatory Cells ◽  
Cell Number ◽  
Chronic Obstructive ◽  
Model Group ◽  
Down Regulation ◽  
Obstructive Pulmonary Disease ◽  
Pas Staining

Objective: The aim of our research was to evaluate Nrf2 in COPD treatment and relative mechanism by vivo study. Materials: The mice were divided into Normal, Model and CCL16 groups. Measuring Pathology and goblet cell number by HE or AB/PAS staining; Evaluating apoptosis cell number by TUNEL assay; using flow separation to analysis inflammatory cells in difference groups; MAPK and NF-κB(p65) protein expression were evaluated by IHC assay in tissues; Total protein concentration of MUC5AC, Nrf2, Bax and Bcl-2 were evaluated by WB assay. Results: Compared with Normal group, the pathology was deteriorate and goblet cell number were significantly up-regulation in Model group, apoptosis goblet cell number were significantly depressed (P < 0.001), lympbocyte rate and hypertrophic rate were significantly down-regulation and Eosinophils rate, Macrophage rate and Neutrophils rate were significantly up-regulation (P < 0.001, respectively) in Model group. By IHC assay, MAPK and NF-κB(p65) proteins expression significantly increased (P < 0.001, respectively) in Model group; by WB assay, MUC5AC and Bcl-2 protein expression were significantly up-regulation and Nrf2 and Bax proteins expression were significantly down-regulation (P < 0.001, respectively) in Model group. Nrf2 supplement, the COPD were significantly improved with relative inflammatory cells rates significantly improving and relative proteins improving. Conclusion: Nrf2 could improve COPD by inducing goblet cell apoptosis increasing via regulation MAPK/NF-κB(p65) pathway in vivo study.

scholarly journals Anti-Diabetic Effects of the Ethyl-Acetate Fraction of Trichilia catigua in Streptozo-tocin-Induced Type 1 Diabetic Rats

2017 ◽  
Vol 42 (3) ◽  
pp. 1087-1097 ◽  
Author(s):  
Rodrigo Mello Gomes ◽  
Luis Fernando de Paulo ◽  
Cynthia Priscilla do Nascimento Bonato Panizzon ◽  
Camila Quaglio Neves ◽  
Bruna Colombo Cordeiro ◽  
...  
Keyword(s):  
Ethyl Acetate ◽  
Kidney Tissue ◽  
Ethyl Acetate Fraction ◽  
Diabetic Rats ◽  
Diabetic Group ◽  
Male Wistar Rats ◽  
Food And Water Intake ◽  
Pancreas Morphology ◽  
Group D

Background/Aims: Trichilia catigua A. Juss., known as “catuaba” in Brazil, has been popularly used as a tonic for fatigue, impotence and memory deficits. Previously, our group demonstrated that the ethyl-acetate fraction (EAF) of T. catigua has antioxidant and anti-inflammatory effects. The present study evaluated the anti-diabetic activity of EAF in type 1 diabetic rats. Methods: Male Wistar rats were divided into four groups (N: non-diabetic group, D: type 1 diabetic group, NC: non-diabetic + EAF group and DC: type 1 diabetic + EAF group). The latter two groups were treated with 200 mg/kg EAF. Type 1 diabetes was induced by intravenous streptozotocin (STZ) injection (35 mg/kg). Starting two days after STZ injection, EAF was administered daily by gavage for 8 weeks. Results: EAF attenuated body mass loss and reduced food and water intake. EAF improved hyperglycaemia and other biochemical parameters, such as alkaline phosphatase (ALP), alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Furthermore, the number of pancreatic β-cells and the size of the islets had increased by β-cell proliferation in the DC group. EAF promoted reduction in kidney tissue damage in STZ-induced diabetic rats by reduction of renal fibrosis. Conclusion: The present study showed that EAF improves glucose homeostasis and endocrine pancreas morphology and inhibits the development of diabetic nephropathy in STZ-induced diabetic rats.

Influence of exercise on dilatation of the basilar artery during diabetes mellitus

2004 ◽  
Vol 96 (5) ◽  
pp. 1730-1737 ◽  
Author(s):  
William G. Mayhan ◽  
Hong Sun ◽  
Jill F. Mayhan ◽  
Kaushik P. Patel
Keyword(s):  
Nitric Oxide ◽  
Diabetes Mellitus ◽  
Basilar Artery ◽  
Potential Role ◽  
Diabetic Rats ◽  
Cerebrovascular Reactivity ◽  
Oxide Synthase ◽  
Enos Protein

Our goal was to examine whether exercise training alleviates impaired nitric oxide synthase (NOS)-dependent dilatation of the basilar artery in Type 1 diabetic rats. To test this hypothesis, we measured in vivo diameter of the basilar artery in sedentary and exercised nondiabetic and diabetic rats in response to NOS-dependent (acetylcholine) and -independent (nitroglycerin) agonists. To determine the potential role for nitric oxide in vasodilatation in sedentary and exercised nondiabetic and diabetic rats, we examined responses after NG-monomethyl-l-arginine (l-NMMA). We found that acetylcholine produced dilatation of the basilar artery that was similar in sedentary and exercised nondiabetic rats. Acetylcholine produced only minimal vasodilatation in sedentary diabetic rats. However, exercise alleviated impaired acetylcholine-induced vasodilatation in diabetic rats. Nitroglycerin produced dilatation of the basilar artery that was similar in sedentary and exercised nondiabetic and diabetic rats. l-NMMA produced similar inhibition of acetylcholine-induced dilatation of the basilar artery in sedentary and exercised nondiabetic and diabetic rats. Finally, we found that endothelial NOS (eNOS) protein in the basilar artery was higher in diabetic compared with nondiabetic rats and that exercise increased eNOS protein in the basilar artery of nondiabetic and diabetic rats. We conclude that 1) exercise can alleviate impaired NOS-dependent dilatation of the basilar artery during diabetes mellitus, 2) the synthesis and release of nitric oxide accounts for dilatation of the basilar artery to acetylcholine in sedentary and exercised nondiabetic and diabetic rats, and 3) exercise may exert its affect on cerebrovascular reactivity during diabetes by altering levels of eNOS protein in the basilar artery.

Rho-kinase: important new therapeutic target in cardiovascular diseases

2011 ◽  
Vol 301 (2) ◽  
pp. H287-H296 ◽  
Author(s):  
Kimio Satoh ◽  
Yoshihiro Fukumoto ◽  
Hiroaki Shimokawa
Keyword(s):  
Cardiovascular Diseases ◽  
Therapeutic Target ◽  
Kinase Inhibitor ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Rho Kinase ◽  
Inflammatory Cells ◽  
Beneficial Effects ◽  
Kinase Pathway

Rho-kinase (ROCKs) belongs to the family of serine/threonine kinases and is an important downstream effector of the small GTP-binding protein RhoA. There are two isoforms of Rho-kinase, ROCK1 and ROCK2, and they have different functions with ROCK1 for circulating inflammatory cells and ROCK2 for vascular smooth muscle cells. It has been demonstrated that the RhoA/Rho-kinase pathway plays an important role in various fundamental cellular functions, including contraction, motility, proliferation, and apoptosis, leading to the development of cardiovascular disease. The important role of Rho-kinase in vivo has been demonstrated in the pathogenesis of vasospasm, arteriosclerosis, ischemia-reperfusion injury, hypertension, pulmonary hypertension, stroke, and heart failure. Furthermore, the beneficial effects of fasudil, a selective Rho-kinase inhibitor, have been demonstrated for the treatment of several cardiovascular diseases in humans. Thus the Rho-kinase pathway is an important new therapeutic target in cardiovascular medicine.

scholarly journals THE EFFECT OF FLAVONOID PROPOLIS KELULUT (Trigona spp) EXTRACT ON MACROPHAGE CELL NUMBER IN PERIODONTITIS (IN VIVO STUDY IN MALE WISTAR RATE (Rattus novergicus) GINGIVA)

2020 ◽  
Vol 5 (1) ◽  
pp. 28
Author(s):  
Makfiyah Saidah ◽  
Beta Widya Oktiani ◽  
Irham Taufiqurrahman
Keyword(s):  
Inflammatory Cells ◽  
Cell Number ◽  
Negative Control ◽  
Gingival Tissue ◽  
Control Group ◽  
Control Group Design ◽  
Propolis Extract ◽  
Periodontal Tissues ◽  
Macrophage Cells

Background : Periodontitis is a condition where there is an increase in the number of inflammatory cells, namely macrophages in periodontal tissue. Macrophag cell is 12-15μm in oval shape cell with purplish blue cytoplasm and this cell’s function is to phagocytes bacteria and infiltrate gingival tissue. Propolis kelulut contains flavonoid that have an anti-inflammatory effect by suppressing the signal pathway p38 MAPK, JNK 1/2 and NF-kB that it can reduce the number of macrophage cells in inflammatory periodontal tissues. Objective: The purpose of this study was to determine the effect of 0.5 mg dose flavonoid propolis extract on the number of macrophage cells in gingiva wistar rats that have been made into a periodontitis condition. Method: This study used a pure experimental method with a post test only with control group design. There were 9 treatment groups, including flavonoid propolis extract on 1,3,5 days, ibuprofen gel on 1,3,5 days and negative control on 1,3 dan 5 days. Results: There was an effect of giving 0.5 mg flavonoids propolis kelulut extract to the number of macrophage cells in periodontitis. Conclusion: Flavonoid propolis kelulut extract has an effect in increasing the number of macrophage cells on day 3 and decreasing the number of macrophage cells on the 5th day.

Club Cell Secretion Protein 16 (CC16) Improve Chronic Obstructive Pulmonary Disease In Vivo Study

2022 ◽  
Vol 12 (2) ◽  
pp. 279-286
Author(s):  
Zhihong Qiu ◽  
Li Yan ◽  
Juan Xu ◽  
Xiaojun Qian
Keyword(s):  
Protein Expression ◽  
Goblet Cell ◽  
Inflammatory Cells ◽  
Cell Number ◽  
Chronic Obstructive ◽  
Model Group ◽  
Cell Secretion ◽  
Down Regulation ◽  
Club Cell

Purpose: The purpose of this study was to evaluate CC16 in COPD treatment and relative mechanism by vivo study. Materials and methods: The mice were divided into Normal, Model and CC16 groups. Measuring Pathology and goblet cell number by HE or AB/PAS staining; Evaluating apoptosis cell number by TUNEL assay; using flow separation to analysis inflammatory cells in difference groups; MAPK and NF-κB(p65) protein expression were evaluated by IHC assay in tissues; Total protein concentration of MUC5AC, CC16, Bax and Bcl-2 were evaluated by Western Blot (WB) assay. Results: Compared with Normal group, the pathology was deteriorate and goblet cell number were significantly up-regulation in Model group, apoptosis goblet cell number were significantly depressed (P < 0.001), lympbocyte rate and hypertrophic rate were significantly down-regulation and Eosinophils rate, Macrophage rate and Neutrophils rate were significantly up-regulation (P < 0.001, respectively) in Model group. By IHC assay, MAPK and NF-κB(p65) proteins expression were significantly increased (P < 0.001, respectively) in Model group; by WB assay, MUC5AC and Bcl-2 protein expression were significantly up-regulation and CC16 and Bax proteins expression were significantly down-regulation (P < 0.001, respectively) in Model group. CC16 supplement, the COPD were significantly improved with relative inflammatory cells rates significantly improving and relative proteins improving. Conclusion: CC16 could improve COPD by inducing goblet cell apoptosis increasing via regulation MAPK/NF-κB(p65) pathway In Vivo study.

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