scholarly journals Protective Effects and Mechanisms of Rosuvastatin on Acute Kidney Injury Induced by Contrast Media in Rats

2020 ◽  
Vol 2020 ◽  
pp. 1-6
Author(s):  
Zehui Jiang ◽  
Jun Zhang ◽  
Yuanan Lu
Keyword(s):  
Protective Effect ◽  
Contrast Medium ◽  
Renal Injury ◽  
Intervention Group ◽  
Inflammatory Factors ◽  
Control Group ◽  
Renal Tubules ◽  
Protective Effects ◽  
Sod Activity ◽  
Biochemical Indicators

Objective. To explore the protective effect and mechanism of rosuvastatin on acute renal injury induced by a nonionic hypotonic contrast medium in rats. Methods. Forty-eight healthy adult SD rats were randomly divided into three groups: normal control group (NC); contrast medium control group (CM); and rosuvastatin intervention group (RI). The RI group was intragastrically administered with a 10 mg/kg of rosuvastatin 12 h prior to the contrast exposure. All rats in CM and RI groups were inoculated with 10 mL/kg of chemical (IV) while the same volume of saline for the NC group. At 24 h and 72 h posttreatments, pathomorphological changes of renal tubules were documented, respectively, and several biochemical indicators were tested to assess renal injury of experimental rats. Results. Compared with the CM group, rats in the RI group showed significantly reduced injury of kidneys and decreased levels of biochemical indicators such as blood Scr, blood Cys-C, urine NAG, urine α1-MG, and urine mALB. The serum Hs-CRP in the CM group increased significantly from 24 h to 72 h (p<0.05), but this was not observed in the rats of the RI group. In addition, SOD activity in the RI group was significantly increased (p<0.01) while SOD activity in renal tissue decreased significantly with time in the CM group (p<0.05). Conclusion. Short-term intervention with rosuvastatin can lead to reduced kidney damage associated with the contrast agent by reducing the levels of inflammatory factors and oxidative stress. Thus, rosuvastatin intervention has a protective effect on rats from contrast-induced nephropathy.

Abstract 309: Role of Hemeoxygenase in the Reno-Protective Effects of Soluble Epoxide Hydrolase Inhibition In Diabetic Spontaneously Hypertensive Rats

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Ahmed A Elmarakby ◽  
Jessica Faulkner ◽  
Chelsey Pye ◽  
Babak Baban ◽  
Katelyn Rouch ◽  
...  
Keyword(s):  
Protective Effect ◽  
Renal Injury ◽  
Renal Fibrosis ◽  
Spontaneously Hypertensive Rats ◽  
Epoxide Hydrolase ◽  
Soluble Epoxide Hydrolase ◽  
Control Group ◽  
Protective Effects ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

We previously showed that inhibition of soluble epoxide hydrolase (sEH) increased epoxyeicosatrienoic acids (EETs) levels and reduced renal injury in diabetic mice and these changes were associated with induction of hemeoxygenase-1 (HO-1). The present study determines whether the inhibition of HO negates the reno-protective effect of sEH inhibition in diabetic spontaneously hypertensive rats as a model of diabetic nephropathy in which hypertension coexists with diabetes. After six weeks of induction of diabetes with streptozotocin, SHR were divided into the following groups: untreated, treated with the sEH inhibitor, trans -4-[4-(3-adamantan-1-yl-ureido)-cyclohexyloxy]-benzoic acid (AUCB), treated with the HO inhibitor, stannous mesoporphyrin (SnMP), and treated with both inhibitors for four more weeks; non diabetic SHR served as a control group. Although inhibition of sEH increased renal EETs/DHETEs ratio and HO-1 activity in diabetic SHR, it did not significantly alter blood pressure (plasma EETs/DHETEs ratio was 0.5± 0.1 in AUCB-treated vs. 0.1± 0.01 in untreated diabetic SHR, P<0.05). Treatment of diabetic SHR with AUCB reduced the elevation in urinary albumin and nephrin excretion (albuminuria was 6.5± 0.5 in AUCB-treated diabetic SHR vs. 9± 1.7 mg/day in untreated diabetic SHR and nephrinuria was 70±11 in AUCB-treated diabetic SHR vs. 111± 9 μg/day in untreated diabetic SHR, P<0.05) whereas co-administration of SnMP with AUCB prevented these changes (albuminuria was 10.6± 0.6 mg/day and nephrinuria was 91±11 μg/day). Immunohistochemical analysis revealed elevations in renal fibrosis and apoptosis as evidenced by increased renal TGF-β, fibronectin and annexin V expression in diabetic SHR and these changes were reduced with sEH inhibition. Co-administration of SnMP with AUCB prevented its ability to reduce renal fibrosis and apoptosis in diabetic SHR. In addition, SnMP treatment also prevented AUCB-induced decreases in renal macrophage infiltration and renal TGF-β, NFκB and MCP-1 levels in diabetic SHR. These data suggest that HO-1 induction is involved in the protective effect of sEH inhibition against diabetic renal injury.

scholarly journals Protective effect of dexmedetomidine on kidney injury of parturients with preeclampsia undergoing cesarean section: a randomized controlled study

2019 ◽  
Vol 39 (5) ◽  
Author(s):  
Qing-lin Zhang ◽  
Lei Wang ◽  
Ming-jun Xu ◽  
Tian-long Wang
Keyword(s):  
Blood Pressure ◽  
Cesarean Section ◽  
Intervention Group ◽  
Kidney Injury ◽  
Visual Analogue Score ◽  
Inflammatory Factors ◽  
Controlled Study ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Protective Effects

AbstractThe present study aimed to elucidate the effects of dexmedetomidine on kidney injury of parturients with preeclampsia (PE) undergoing cesarean section. Total 134 cesarean delivery women with PE were randomly divided into intervention group (IG) and control group (CG). Both groups underwent combined spinal and epidural anesthesia (CSEA), the IG was treated with 0.4 μg/(kg·min) dexmedetomidine for 10 min before surgery. The CG was treated with equivalent saline. Heart rate (HR), blood pressure, oxygen saturation (SpO2) of the two groups were measured at different time point after administration. Level of inflammatory factors were detected by enzyme-linked immunosorbent assay (ELISA). Visual analogue score (VAS), Ramsay sedation score (RSS), and kidney injury related indexes were evaluated at different time points. The plasma-drug concentration of patients was determined by High Performance Liquid Chromatography (HPLC) method. Compared with CG, HR, PE, and diastolic blood pressure (DBP) showed lower level while SpO2 showed higher level in IG. Furthermore, expression of tumor necrosis factor α (TNF-α), interleukin-6 (IL-6), and IL-10 in IG was decreased after drug administration, the contents of β2-MG, KIM-1 and urine protein were also decreased in contrast to the CG (all P<0.05). Besides, VAS score was decreased but Ramsay score was increased in the IG (both P<0.05). The results of HPLC showed that the half life of dexmedetomidine was about 20 min and it is speculated that the drug can be quickly metabolized within 24 h. Dexmedetomidine exerted protective effects on kidney injury of parturients with PE undergoing cesarean section.

Analysis of the Protective Effect of Interleukin-5 On Sepsis Mice

2021 ◽  
Vol 7 (5) ◽  
pp. 1638-1645
Author(s):  
Xiaokun Wang ◽  
Fuyang Pei ◽  
Xiaoping Song ◽  
Hongmei Wang
Keyword(s):  
B Cells ◽  
Protective Effect ◽  
Intervention Group ◽  
Protective Role ◽  
Inflammatory Factors ◽  
Control Group ◽  
Response Factors ◽  
Interleukin 5 ◽  
Proliferation And Differentiation ◽  
Inflammatory Macrophages

IL-5 can stimulate the growth and differentiation of EOS, inhibit its apoptosis and stimulate the proliferation and differentiation of B cells with other cytokines, and act on mature B cells to promote the synthesis of IgA and IgM. Therefore, this paper takes C57BL / 6 mice as the experimental object to explore the protective effect of interleukin-5 on sepsis mice. The experimental results show that the serum cxcl-1 in sepsis model group is significantly higher than that in control group at each time point, reaching the peak at 12 h, while cxcl-1 in IL-5 intervention group is significantly lower than that in control group. IL-5 can reverse the liver injury induced by CLP in septic mice, the mechanism may be to reduce the production of inflammatory factors in the liver, and the liver function of mice was not damaged 12 hours after sepsis. IL-4 and IL-13 of type 2 inflammatory response factors can promote the conversion of macrophages to anti-inflammatory macrophages, inhibit the inflammatory reaction, and play a protective role in sepsis.

scholarly journals Protective Effects of Adiponectin Against Diabetic Renal Injury in a Mouse Model of Diabetes

2017 ◽  
Vol 43 (2) ◽  
pp. 870-878 ◽  
Author(s):  
Jiacai Hu ◽  
Junjun Dong ◽  
Zhijie Yang ◽  
Hao Wu ◽  
Na Yang
Keyword(s):  
Blood Glucose ◽  
Renal Injury ◽  
Fasting Blood Glucose ◽  
Kidney Cortex ◽  
Control Group ◽  
High Dose ◽  
Protective Effects ◽  
Model Group ◽  
Β Cells ◽  
Sod Activity

Background/Aims: Adiponectin (Apn) has shown anti-diabetic and anti-inflammatory potential. In the study, we studied and tested the protective effects of Apn against diabetic renal injury and the possible mechanism of these effects. Methods: After 1 week of adaptive feeding, 30 mice were randomly divided into 5 groups: the control group, the model group, the Apn (L) group, the Apn (M) group and the Apn (H) group. All mice were marked and weighed. Following 4 weeks of a pro-diabetic high-fat diet, the model group and Apn groups were injected intraperitoneally with a high dose of STZ (85 mg/kg), while the normal control group was injected with sodium citrate. Fasting blood glucose was measured daily, starting 3 days after STZ injection. After confirming the success of the diabetic model by measuring blood glucose of more than 16.7 nM for 3 successive days, we observed the animal models for an additional 4 weeks. After body weights were measured, urinary albumin, urinary protein, SOD activity and malondialdehyde (MDA) were measured by ELISA, BCA and biochemical assay respectively . Moreover, plasma insulin was assayed by radioimmunoassay, insulin expression in pancreatic β cells was assayed by immunohistochemistry and receptor for advanced glycation end products (RAGE) and corresponding PKC and PKA signaling in the kidney cortex were also assayed by Western blot and Real-time PCR. Results: The results showed that Apn can significantly reduce MDA and enhance SOD activity. Moreover, Apn promoted the synthesis and secretion of insulin by islet β-cells and reduced RAGE accumulation in the kidney, which was associated with down-regulated PKC expression and upregulated PKA expression. Conclusion: Apn has protective effects against hyperglycemia and can effectively enhance antioxidation, promote the secretion of insulin and reduce the accumulation of glycosylated products in T2DM mice; these effects were associated with inhibition of PKC and promotion of PKA signaling.

Protective effect of vanillin against carbon tetrachloride (CCl4)-induced oxidative brain injury in rats

2011 ◽  
Vol 28 (7) ◽  
pp. 655-662 ◽  
Author(s):  
Mohamed Makni ◽  
Yassine Chtourou ◽  
Mohamed Barkallah ◽  
Hamadi Fetoui
Keyword(s):  
Carbon Tetrachloride ◽  
Protective Effect ◽  
Brain Damage ◽  
Glutathione Transferase ◽  
Single Injection ◽  
Male Rats ◽  
Control Group ◽  
Protective Effects ◽  
Degree Of Protection ◽  
Oxidative Brain Injury

This study investigated the protective effects of vanillin against acute brain damage induced by carbon tetrachloride (CCl4) in rats. The study was performed on 32 male rats divided into four groups: a control group, vanillin group ([Va] 150 mg/kg/day, intraperitoneally [i.p.]) and CCl4 toxication groups received a single injection of CCl4 (1 ml/kg, i.p.; CCl4 and Va + CCl4 groups). The degree of protection in brain tissue was evaluated by the levels of malondialdehyde (MDA), glutathione (GSH), superoxide dismutase, glutathione transferase, glutathione peroxidase and nitric oxide (NO). Vanillin showed a significant brain-protective effect by decreasing the level of lipid peroxidation and NO2 and elevated the activities of antioxidative enzymes and level of GSH. Consequently vanillin blocked oxidative brain damage induced by CCl4 in rats.

P0522INHIBITING 15-PGDH PREVENTS ISCHEMIC RENAL INJURY BY A PGE2/EP4 SIGNALING PATHWAY MEDIATING VASODILATION, INCREASED RENAL BLOOD FLOW, AND INCREASED ADENOSINE/A2A RECEPTOR

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Byeong Woo KIm ◽  
Sun hee Kim ◽  
Ki beom Bae
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Renal Injury ◽  
Ischemia Reperfusion ◽  
Adenosine A2a Receptor ◽  
Vehicle Group ◽  
Control Group ◽  
Protective Effects ◽  
A2a Receptor ◽  
Adenosine A2a

Abstract Background and Aims We demonstrate the marked activity of SW033291, an inhibitor of 15-hydoxyprostaglandin dehydrogenase (15-PGDH), in preventing acute kidney injury (AKI) in a murine model of ischemia reperfusion injury (IRI). AKI due to ischemic injury represents a significant clinical problem. Prostaglandin E2 (PGE2) is vasodilator in the kidney, but is rapidly degraded in vivo due to catabolism by 15-PGDH. We investigated the potential of SW033291, a potent and specific 15-PGDH inhibitor, as prophylactic treatment for ischemic AKI. Method 10-week aged male C57/BL6 mice were randomly allocated to five groups (n=8 to 15 in each group): the sham-control group, sham-SW033291 group, IRI-vehicle group, IRI-indomethacin group and the IRI-SW033291 group. IRI were induced by clamping bilateral renal artery for 30 min followed by 24 hours of reperfusion. Vehicle, indomethacin, or SW033291 were intraperitoneally administered three times at 1 hour before, immediately after, and 12 hours after IRI. Renal function, histological changes, and renal blood flow were compared and the relevant parameters of oxidative stress and inflammation were detected. Results Prophylactic administration of SW033291 significantly increased renal tissue PGE2 levels and increased post-AKI renal blood flow and renal arteriole area. In parallel, prophylactic SW033291 decreased post-AKI histologic injury score and tubular apoptosis and markedly reduced biomarkers of renal injury that included BUN, creatinine, NGAL and KIM-1. Prophylactic SW033291 also reduced post-AKI induction of proinflammatory cytokines, high mobility group box 1 (HMGB1), and malondialdehyde (MDA). Protective effects of SW033291 were mediated by PGE2 signaling as they could be blocked by pharmacologic inhibition of PGE2 synthesis or of the EP4 type PGE2 receptor. Consistent with activation of PGE2 signaling, SW033291 induced renal levels of both EP4 and of cyclic adenosine monophosphate (cAMP), along with other vasodilatory effectors including AMP, adenosine, and the adenosine A2A receptor (A2A). Protective effects of SW0333291 could largely be achieved with a single prophylactic dose of the drug. Conclusion Inhibiting 15-PGDH may thus represent a novel strategy for prophylaxis of ischemic AKI in multiple clinical settings, including renal transplantation and cardiovascular surgery.

scholarly journals Mechanism of SQQX Decoction’s Protective Effect on SHR: A Serum Metabolomics-Based Analysis

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Jiayun Wu ◽  
Lingling Li ◽  
Lin Li ◽  
Yanjun Li ◽  
Xiang Xiao ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Protective Effect ◽  
Metabolic Profiling ◽  
Transforming Growth Factor ◽  
Cholesterol Metabolism ◽  
Pharmaceutical Preparation ◽  
Intervention Group ◽  
Partial Least Square ◽  
Control Group ◽  
Optimal Dosage

SangQiQingXuan (SQQX) decoction is a pharmaceutical preparation exerting good therapeutic efficacy on high blood pressure (BP) and has widely been accepted in primarily hypertensive patients as a herbal formula prescribed by Professor Li Huang from China-Japan Friendship Hospital according to her 30-year clinical experience. A previous study showed that SQQX could reduce BP by decreasing levels of many inflammatory factors such as transforming growth factor beta (TGFβ) and elevating peroxisome proliferator activated receptor (PPAR) expression. However, a research focusing on SQQX’s protection against HTN from a metabolomic perspective has never been done before. This study aimed to figure out the metabolic profiling variations due to oral administration of SQQX in spontaneous hypertensive rat (SHR) models and to find out the optimal dosage of SQQX. SHR in the intervention group orally received SQQX extract of three doses, namely, the low- (5.25 g/kg/d), middle- (10.5 g/kg/d), and high-dosage groups (21 g/kg/d) for 90 days. Rats were sacrificed at the end of the experiment, and their serum was collected for further examination. Serum metabolic profiling variations were analyzed using ultraperformance liquid chromatography coupled with tandem mass spectrometry (UPLC/MS). Results showed that dealing with SQQX remarkably decreased systolic blood pressure (SBP) of SHRs and the high-dosage group was with the best therapeutic effect where a total of 11 metabolites were markedly changed in contrast to the model group. Orthogonal partial least square discriminant analysis (OPLS-DA) score plot showed that the 5 groups of serum samples were divided into 5 categories, and the metabolic trajectory of the high-dosage SQQX group was inclined to move to the control group. Glycochenodeoxycholic acid, nicotinamide-N-oxide, and tryptophan betaine might be biomarkers that specifically marked the protective effects of SQQX against high BP mainly involving in cholesterol metabolism, primary bile acid biosynthesis, bile secretion, and nicotinate and nicotinamide metabolism. To conclude, SQQX has a protective effect on SHR, which may be partially correlated to restoration of perturbed metabolism in serum.

scholarly journals Effects of clinoptilolite (zeolite) on attenuation of lipopolysaccharide-induced stress, growth and immune response in broiler chickens

2015 ◽  
Vol 15 (3) ◽  
pp. 681-697 ◽  
Author(s):  
Qiu Jue Wu ◽  
Qin Yu Wang ◽  
Tian Wang ◽  
Yan Min Zhou
Keyword(s):  
Growth Performance ◽  
Broiler Chickens ◽  
Intestinal Morphology ◽  
Control Group ◽  
Protective Effects ◽  
Gut Health ◽  
Ileal Mucosa ◽  
Sod Activity ◽  
Lps Challenge ◽  
Natural Clinoptilolite

Abstract The effects of natural clinoptilolite (NCLI) and modified clinoptilolite (MCLI) were evaluated in broilers challenged with lipopolysaccharide (LPS) in a 21-d feeding trial. A total of 288 one-day-old chickens were allocated into three treatment groups: control, NCLI (2%) and MCLI (2%). Half of the birds from each treatment group were challenged with either 0.9% NaCl solution or LPS (250 μg/kg body weight, orally administered) at 16, 18 and 21 d of age. Before the LPS challenge, no dietary effect on bird growth performance was found (P>0.05). When LPS was orally administered, no significant changes in growth performance of broilers was found (P>0.05). However, small intestinal morphology and development, malondialdehyde (MDA) content of the jejunual and ileal mucosa, and superoxide dismutase (SOD) activity of the ileal mucosa were significantly affected (P<0.05). Supplementation with NCLI and MCLI significantly decreased the MDA contents of the jejunual and ileal mucosa and improved the SOD activity of the ileal mucosa and the development of the small intestine compared with the control group (P<0.05). The results indicated that NCLI and MCLI additions in feed had protective effects on the gut health of broilers against LPS challenge.

scholarly journals Protective Effects of Chinese Traditional Medicine Buyang Huanwu Decoction on Myocardial Injury

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Guangde Yang ◽  
Zhiyuan Fang ◽  
Yu Liu ◽  
Hui Zhang ◽  
Xiaolian Shi ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Myocardial Ischemia ◽  
Protective Effect ◽  
Myocardial Injury ◽  
Control Group ◽  
Protective Effects ◽  
Buyang Huanwu Decoction ◽  
Pre Treatment ◽  
Cluster Of Differentiation ◽  
Electrocardiogram Ecg

Many clinical studies have reported that Buyang Huanwu Decoction (BYHWD) has a protective effect on ischemic heart disease (IHD). In the present study, the protective effect of BYHWD on myocardial ischemia was investigated. Different doses of BYHWD and Compound Danshen Dropping Pills (CDDP) were lavaged to rats, respectively, isoproterenol (ISO) was intraperitoneally injected in to all animals to induce myocardial ischemia except the control group. Electrocardiogram (ECG) of each animal was recorded; activities of lactate dehydrogenase (LDH), creatine kinase (CK) and aspartate aminotransferase (AST) in serum were detected. As the results of ECG showed, pre-treatment with BYHWD inhibited ischemic myocardial injury, and the activities of LDH, CK and AST were lower than those in the myocardial ischemia model group, which suggests that BYHWD rescues the myocardium from ischemia status. To research the potential mechanism, the level of nitric oxide (NO), nitric oxide syntheses (NOS) and inducible nitric oxide syntheses (iNOS), the expression of iNOS and ligand of cluster of differentiation 40 (CD40L) were detected. The results revealed that BYHWD significantly decreased the level of NO, NOS and iNOS in serum. Moreover, BYHWD decreased the expression of iNOS and CD40L in myocardial tissues. These results indicate that the protective effect of BYHWD on myocardial ischemia and mechanism are associated with inhibition of iNOS and CD40L expression.

scholarly journals Effects of oral and intraperitoneal magnesium treatment against cadmium-induced oxidative stress in plasma of rats

2012 ◽  
Vol 63 (3) ◽  
pp. 247-254 ◽  
Author(s):  
Aleksandra Buha ◽  
Zorica Bulat ◽  
Danijela Đukić-Ćosić ◽  
Vesna Matović
Keyword(s):  
Oxidative Stress ◽  
Rat Plasma ◽  
Control Group ◽  
Protective Agent ◽  
Protective Effects ◽  
Negative Effects ◽  
Sod Activity ◽  
Total Oxidative Status ◽  
Intraperitoneal Treatment ◽  
Induced Changes

Cadmium (Cd) has been recognised as one of the most important environmental and industrial pollutants, and up-to-date investigations have shown that one of the mechanisms of its toxicity is associated with the induction of oxidative stress. The aim of this study was to determine the connection between acute oral and intraperitoneal exposure to Cd and parameters indicative of oxidative stress in the plasma of rats, as well as to examine the potential protective effect of magnesium (Mg) in conditions of acute oral and intraperitoneal Cd poisoning. The experiment was performed on male albino Wistar rats (n=40) randomly divided into control group, Cdor group that received 30 mg kg-1 b.w. Cd by oral gavage, Cd+Mgor group that orally received 50 mg kg-1 b.w. Mg one hour before oral Cd, Cdip group that received 1.5 mg kg-1 b.w. Cd intraperitoneally, and Cd+Mgip group that intraperitoneally received 3 mg kg-1 b.w. Mg 10 min before intraperitoneal Cd. The animals were sacrifi ced 24 h after treatment and the following parameters were measured: superoxidedismutase activity, superoxide anion, total oxidative status, advanced oxidation protein products, and malondialdehyde. All parameters of oxidative stress in rat plasma were negatively affected by Cd treatment with more pronounced negative effects after intraperitoneal treatment, with the exception of superoxide dismutase (SOD) activity. Although both oral and intraperitoneal Mg pretreatment had protective effects, more pronounced benefi cial effects were observed after oral administration, since it managed to completely prevent Cd-induced changes in the investigated parameters. The observed results support the use of Mg as potential protective agent against toxic effects caused by Cd.

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