Ligusticum chuanxiong Effects on Oxidative Stress and Nrf2/HO-1 Signaling Using Nano-Magnetic Beads in Bleomycin-Induced Renal Fibrosis Rats

2020 ◽  
Vol 12 (10) ◽  
pp. 1185-1191
Author(s):  
Haixia Liu ◽  
Wenwen Huang ◽  
Xinli Han ◽  
Qihang Ma
Keyword(s):  
Renal Fibrosis ◽  
Magnetic Beads ◽  
Rat Kidney ◽  
Smooth Muscle Actin ◽  
Kidney Tissue ◽  
Renal Tissue ◽  
High Dose ◽  
Early Administration ◽  
Ligusticum Chuanxiong ◽  
Hematoxylin Eosin

Ligusticum chuanxiong can relieve the degree of renal fibrosis. However, the specific mechanism of Ligusticum chuanxiong to improve renal fibrosis is not yet clear. A unilateral ureteral obstruction was used to construct a rat renal fibrosis model. The rats were treated with 20 mg/kg and 40 mg/kg of Ligusticum chuanxiong. Four weeks after treatment, blood was collected from the rats, and the rats were sacrificed. Blood urea nitrogen (BUN), serum creatinine (Scr), kidney tissue malondialdehyde (MDA), and superoxide dismutase (SOD) levels were detected. Hematoxylin–eosin staining was used to observe the pathological rat kidney changes. The renal tissue smooth muscle actin (α-SMA) was detected by immunohistochemistry. Nrf2 and HO-1 levels were determined by PCR using nano-magnetic beads. The results showed BUN, Scr, and MDA levels reduced, while SOD levels were elevated in Ligusticum chuanxiong-treated rats, compared to model rats (P < 0.05). These effects were more dramatic in Ligusticum chuanxiong high dose (HD) rats compared to Ligusticum chuanxiong low dose (LD) rats. Additionally, Nrf2 and HO-1 levels were elevated in Ligusticum chuanxiong-treated rats (P < 0.05). These effects were also more dramatic in HD rats compared to LD rats. These findings indicated that Ligusticum chuanxiong early administration can reduce renal fibrosis in rats by stimulating the Nrf2/HO-1 pathway.

scholarly journals Intervention Effect of Compatibility of Salvianolic Acid A & B on PDGF-C/PDGFR-α Signaling Pathway in Renal Fibrosis

2015 ◽  
Vol 4 (2) ◽  
pp. 13
Author(s):  
Bin Yu
Keyword(s):  
Signaling Pathway ◽  
Renal Fibrosis ◽  
Kidney Tissue ◽  
Renal Tissue ◽  
Salvianolic Acid B ◽  
Control Group ◽  
Salvianolic Acid ◽  
Salvianolic Acid A ◽  
Drug Compatibility ◽  
Renal Tubular

<strong>Objective</strong>: To explore the effect of salvianolic acid A &amp; B component molecules of drug compatibility on PDGF-c/PDGFR-α signaling pathway in renal fibrosis of rats. <strong>Methods</strong>: 40 male SPF SD rats were randomly divided into four groups: control group, salvianolic acid A group, salvianolic acid B group and salvianolic acid A + B group, with 10 rats in each group. Each group was treated for two weeks. After the intervention, samples were collected. And scores of HE and Masson was compared. The expression of PDGF-c/PDGFR-α in rental tissue in them was also tested and compared.<strong> Results</strong>: Compared with the control group, the score of HE and Masson in intervention groups was markedly decreased, and scores in salvianolic acid B group and salvianolic acid A + B group were reduced significantly (<em>p </em>&lt; 0.05); Compared with the control group, the expression of PDGF-c/PDGFR-α in rental tissue in intervention groups was lower(<em>p </em>&lt; 0.05), especially in salvianolic acid B group and salvianolic acid A + B group (<em>p </em>&lt; 0.05).<strong>Conclusion</strong>: salvianolic acid A &amp; B component molecules of drug compatibility could significantly improve the pathological changes in the kidney tissue of rats, suppress the expression of PDGF-c/PDGFR-α in renal tissue, and improve the renal function, renal tubular function and renal pathology.

Effect of potassium concentration and ouabain on the renal adaptation to potassium depletion in isolated perfused rat kidney

1986 ◽  
Vol 64 (11) ◽  
pp. 1427-1433 ◽  
Author(s):  
Daniel B. Ornt
Keyword(s):  
Sodium Excretion ◽  
Rat Kidney ◽  
Control Diet ◽  
Kidney Tissue ◽  
Renal Tissue ◽  
Renal Adaptation ◽  
Low K ◽  
K Depletion ◽  
Isolated Kidneys

Renal adaptation for potassium (K) conservation has been demonstrated in isolated perfused kidneys from rats within 3 days of K depletion and appears to be independent of aldosterone and sodium excretion. This study was designed to investigate whether the renal adaptation for K conservation is independent of ambient [K] and renal tissue levels of K and whether ouabain may have effects on K excretion, which are in constrast to the effects on K excretion in normal animals, in the first study, rats K depleted for 3 days received 2500 μequiv. KCl intraperitoneally, while other K-depleted rats and a group of control diet animals received intraperitoneal H2O alone to determine whether simple restoration of K deficits would reverse the renal adaptation for K conservation. Intraperitoneal KCl increased plasma [K] and kidney tissue K significantly within 3 h in the K-repleted group compared with the K-depleted rats. Isolated kidneys were perfused from the three groups of rats 3 h after intraperitoneal injection. Despite K repletion in vivo, perfused kidneys from the K-repleted group still had significantly decreased K excretion (1.28 ± 0.085 μequiv./min) compared with controls (2.05 ± 0.291 μequiv./min), and K excretion was still not different from the K-depleted group (0.57 ± 0.134 μequiv./min). However, fractional K excretion by the kidneys from K-repleted rats was increased above K-depleted kidneys (0.48 ± 0.051 vs. 0.18 ± 0.034, p < 0.01). Despite the increased renal tissue K in K-repleted kidneys at the start of perfusion (285 ± 5.1 vs. 257 ± 5.4 μequiv./g), by the end of the perfusion tissue K in perfused kidneys was identical in all three groups. In the second study, isolated kidneys were perfused from 3-day K-depleted or control rats with either 2 or 6 mM [K] in the perfusate. Isolated kidneys adapted to 3 days of K depletion excreted less K at both 2 and 6 mM [K] compared with controls at the same ambient [K]. The linear relationship of K excretion to perfusate [K] was significantly different in controls compared with low K adapted kidneys (p < 0.001). Finally, when 10−4 M ouabain was added after 60 min of perfusion in kidneys from control diet rats, there was a sodium diuresis and fractional K excretion decreased significantly (0.55 ± 0.043 to 0.32 ± 0.044, p < 0.01). However, in low K adapted kidneys, ouabain had no effect on fractional K excretion (0.020 ± 0.051 to 0.18 ± 0.038) despite a similar increase in sodium excretion. Perfusions of kidneys from 3-day K-depleted rats at 4 × 10−3 M ouabain gave similar results, showing no change in fractional K excretion. Low K adaptation to K depletion developed within 3 days and was not totally abolished by acute K repletion. Maneuvers that favored either a decrease in renal tissue K or an increase in tissue K did not reverse low K adaptation, although renal tissue K levels did alter the rate of K excretion in both controls and K-depleted kidneys. Therefore, a reduction in tissue K was clearly not the sole mediator of renal K conservation. Finally, the markedly different response of low K adapted kidneys to ouabain compared with controls strongly suggests a mechanism for K reabsorption that developed within 3 days of K depletion and is ouabain sensitive.

scholarly journals Niao Du Kang Mixture Increases the Expression of mir-129-5p to Relieve Renal Fibrosis

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Yan-lin Li ◽  
Lin-na Liu ◽  
Lin Huang ◽  
Hai-wen An ◽  
Jian-lin Jian ◽  
...  
Keyword(s):  
Renal Fibrosis ◽  
Interstitial Fibrosis ◽  
Cell Model ◽  
Rat Kidney ◽  
Kidney Tissue ◽  
Urine Protein ◽  
Renal Interstitial Fibrosis ◽  
Expression Levels ◽  
Qrt Pcr

Objective. To investigate the efficacy of Niao Du Kang (NDK) mixture in renal fibrosis of rats and to explore the mechanism underlying the effect of NDK on renal fibrosis. Methods. Unilateral ureteral obstruction (UUO) was used to replicate a rat renal interstitial fibrosis model. The drug-administered groups were given 20 ml/kg (NDK-H), 10 ml/kg (NDK-M), and 5 ml/kg (NDK-L) NDK mixture once a day for 21 days beginning 48 hours after surgery. The 24-hour urine protein and serum creatinine (CR) levels in the sham group rats, UUO rats, and NDK mixture-treated rats were measured after the last administration. The pathological changes of rat kidney tissue were observed by HE staining. The degree of fibrosis was observed by Masson’s staining and scored. The expression levels of TGF-β, α-SMA mRNA, and mir-129-5p in kidney were detected by qRT-PCR. HK-2 cells were treated with 5 ng/ml TGF-β to induce HK-2 cell fibrosis. The expression levels of TGF-β, α-SMA mRNA, and mir-129-5p in HK-2 cells were detected by qRT-PCR. TargetScan predicted the target gene of mir-129-5p, HK-2 cells were transfected with mir-129-5p mimic, and an overexpressed mir-129-5p HK-2 cell model was constructed. qRT-PCR was used to detect the expression of PDPK1 mRNA. Western blot was used to detect the expression of PDPK1, AKT, and p-AKT in HK-2 cells induced by TGF-β and in UUO rats. Results. NDK mixture significantly reduced the 24-hour urine protein and CR levels of UUO rats. HE staining showed that the NDK mixture group exhibited a significantly reduced degree of renal interstitial fibrosis. NDK mixture also reduced the expression of TGF-β and α-SMA, and the middle-dose group showed a better therapeutic effect. In vitro studies showed that NDK mixture-containing serum increased the expression of mir-129-5p to reduce renal fibrosis. In addition, NDK mixture increased the expression of mir-129-5p in vivo. Further studies indicated that mir-129-5p could target PDPKl to reduce its expression. The NDK-containing serum group also exhibited reduced expression of PDPK1. Conclusion. NDK mixture can significantly improve renal function and improve renal fibrosis in UUO model rats. Furthermore, NDK mixture can inhibit the expression of PDPK1 by upregulating the expression of mir-129-5p and then inhibiting the PI3K/AKT pathway to improve renal fibrosis.

scholarly journals MiR-214 promotes renal fibrosis in diabetic nephropathy via targeting SOCS1

2021 ◽  
Vol 18 (5) ◽  
pp. 1009-1015
Author(s):  
Weiwei Xi ◽  
Xuming Zhao ◽  
Meijun Wu ◽  
Xueqin Fu ◽  
Wenjuan Jia ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Renal Fibrosis ◽  
Quantitative Polymerase Chain Reaction ◽  
Kidney Tissue ◽  
Renal Tissue ◽  
Luciferase Reporter ◽  
Cytokine Signaling ◽  
Suppressor Of Cytokine Signaling ◽  
Marker Proteins ◽  
Fibrosis Marker

Purpose: To elucidate how miR-214 regulates the pathogenesis of diabetic nephropathy (DN). Methods: The extent of fibrosis in DN mice kidneys was examined using Masson’s staining. Quantitative polymerase chain reaction (qPCR) was used to determine the levels of miR-214. Dual luciferase reporter assay was used to identify the target of miR-214. The expression of fibrosis marker proteins of high glucose-stimulated NRK-52E cells transfected with miR-214 was determined using western blotting. Results: Fibrosis in renal tissue of DN mice was significantly increased and miR-214 was upregulated (p < 0.001). Suppressor of cytokine signaling 1 protein (SOCS1) was the target gene of miR-214, and overexpression of miR-214 promoted fibrosis (p < 0.05, p < 0.001). On the other hand, overexpression of SOCS1 inhibited this process, indicating that miR-214 promoted fibrosis via targeting SOCS1 (p < 0.001). Finally, inhibition of miR-214 c ameliorated renal fibrosis in DN mice (p < 0.01, p < 0.001). Conclusions: MiR-214 is upregulated in db/db DN mice kidney tissue; miR-214 regulates renal fibrosis in DN mice by targeting SOCS1.

scholarly journals Comparison of the phosphate-dependent glutaminase obtained from rat brain and kidney

1985 ◽  
Vol 229 (2) ◽  
pp. 399-408 ◽  
Author(s):  
W G Haser ◽  
R A Shapiro ◽  
N P Curthoys
Keyword(s):  
Rat Brain ◽  
Rat Kidney ◽  
Kidney Tissue ◽  
Brain Mitochondria ◽  
Renal Tissue ◽  
Hill Coefficient ◽  
Brain Extract ◽  
Maximal Activation ◽  
The Difference ◽  
A Minor

A phosphate-dependent glutaminase was purified 1200-fold from rat brain. In the absence of a polyvalent anion, the glutaminase exists as an inactive protomer which has an estimated Mr of 126000. The addition of 100mM-phosphate causes maximal activation and a dimerization (Mr 249000) of the glutaminase. The phosphate activation is sigmoidal, with a K0.5 of 25mM and a Hill coefficient (h) of 1.5 Glutamate inhibition is competitive with respect to glutamine and is decreased by increasing the concentration of phosphate. Phosphate also decreases the Km for glutamine. The purified glutaminase contains a predominant peptide (Mr 65000) and a minor peptide (Mr 68000) that are present in an approximate ratio of 4:1 respectively. The glutaminase immunoprecipitated from freshly solubilized brain tissue or from synaptosomal and non-synaptosomal brain mitochondria contains the same distribution of the two peptides. In contrast, the glutaminase purified from rat kidney contains five to seven peptides that range in Mr value from 59000 to 48000, and immunoprecipitates derived from freshly solubilized renal tissue contain only the Mr-65000 peptide. Partial proteolysis and size fractionation of the three immunoprecipitated peptides indicate that they are structurally related. The series of peptides characteristic of the purified renal glutaminase is generated on storage of the solubilized extract of kidney tissue. The glutaminase contained in the solubilized brain extract is not degraded unless a renal extract is added. Thus the difference in the pattern of peptides associated with the two purified enzymes is due to an endogenous renal proteinase that is not present in brain.

Roflumilast, a phosphodiesterase 4 inhibitor, attenuates cadmium-induced renal toxicity via modulation of NF-κB activation and induction of NQO1 in rats

2019 ◽  
Vol 38 (5) ◽  
pp. 588-597 ◽  
Author(s):  
MN Ansari ◽  
RI Aloliet ◽  
MA Ganaie ◽  
TH Khan ◽  
Najeeb-ur-Rehman ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protective Effect ◽  
Urine Volume ◽  
Kidney Tissue ◽  
Kidney Injury ◽  
Treated Group ◽  
Renal Tissue ◽  
High Dose ◽  
Dependent Manner ◽  
Histopathological Studies

Objective: In the present study, the protective effect of Roflumilast (ROF, a selective phosphodiesterase (PDE-4) inhibitor) was investigated against cadmium (Cd)-induced nephrotoxicity in rats. Methods: A total of 24 rats were selected and randomly divided into four groups ( n = 6). Group 1 served as the control; groups 2–4 administered with CdCl2 (3 mg/kg, i.p.) for 7 days; groups 3 and 4 were co-administered with ROF in doses of 0.5 and 1.5 mg/kg, orally for 7 consecutive days. Nephrotoxicity was evaluated by measuring urine volume, urea and creatinine levels in urine and serum. Oxidative stress was confirmed by measuring malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) levels in kidney tissue followed by histopathological studies. Results: CdCl2 administration results in a significant ( p < 0.01) decrease in urine volume, urea, and creatinine levels in urine, as well as GSH, SOD, and CAT levels in renal tissue. In addition, Cd also produced significantly increased ( p < 0.01) urea and creatinine levels in serum and TBARS levels in renal tissues. Rats treated with ROF significantly ( p < 0.01) restore the altered levels of kidney injury markers, nonenzymatic antioxidant, as well as depleted enzymes in dose-dependent manner. An increased expression of NF-κB p65 and decreased expression of GST and NQO1 in the Cd only treated group were significantly reversed by high dose of ROF (1.5 mg/kg). Histopathological changes were also ameliorated by ROF administration in Cd-treated groups. Conclusion: In conclusion, ROF treatment showed protective effect against renal damage and increased oxidative stress induced by Cd administration.

scholarly journals Endothelial Cell-Specific Molecule 1 Promotes Endothelial to Mesenchymal Transition in Renal Fibrosis

Toxins ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 506 ◽  
Author(s):  
Tung-Wei Hung ◽  
Chao-Yang Chu ◽  
Chen-Lin Yu ◽  
Chu-Che Lee ◽  
Li-Sung Hsu ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Mouse Model ◽  
Renal Fibrosis ◽  
Smooth Muscle Actin ◽  
Kidney Tissue ◽  
Vimentin Expression ◽  
Mesenchymal Transition ◽  
Endothelial To Mesenchymal Transition

The endothelial-to-mesenchymal transition (EndoMT) is involved in the complex pathogenesis of renal fibrosis. The soluble proteoglycan endothelial cell-specific molecule 1 (ESM1) is significantly upregulated in many tumor cells and cirrhosis-related disease. The role of ESM1 in renal fibrosis is unknown. This study investigates the role of ESM1 in renal fibrosis, using an in vivo unilateral ureteral obstruction (UUO) mouse model of renal fibrosis and in vitro mouse kidney MES 13 cells overexpressing ESM1. We observed that ESM1 overexpression significantly increased the motility and migration of MES 13 cells, independent of cell viability. In ESM1-overexpressing MES 13 cells, we also observed elevated expression of mesenchymal markers (N-cadherin, vimentin, matrix metallopeptidase 9 (MMP9)) and the fibrosis marker α-smooth muscle actin (α-SMA) and decreased expression of the endothelial marker vascular endothelial cadherin (VE-cadherin) and CD31. In a mouse model of fibrosis induced by unilateral ureter obstruction, we observed time-dependent increases in ESM1, α-SMA, and vimentin expression and renal interstitial collagen fibers in kidney tissue samples. These results suggest that ESM1 may serve as an EndoMT marker of renal fibrosis progression.

scholarly journals Placental Cryoextract and Renin-Angiotensin-Aldosterone System Blockade Mitigate Renal Failure in Rats

2021 ◽  
Vol 31 (3) ◽  
pp. 223-235
Author(s):  
Mykola Repin ◽  
◽  
Yuliia Chyzh ◽  
Larysa Marchenko ◽  
Tetyana Govorukha ◽  
...  
Keyword(s):  
Renal Failure ◽  
Rat Kidney ◽  
Kidney Tissue ◽  
Renal Tissue ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Excretory Function ◽  
Comprehensive Therapy ◽  
Inflammatory Processes ◽  
The Impact

Here, we have studied the impact of administration of rat placental cryoextract (PCE), drug blockade of the renin-angiotensin-aldosterone system (RAAS) with enalapril and spironolactone and their combination on the rat kidney tissue structure and excretory function at different stages of chronic renal failure (CRF) development using the glycerol model. In 3 weeks after glycerol introduction, the animals from all the groups showed low values of glomerular filtration rate, impaired blood flow in renal cortex, tubular epithelial dystrophy, inflammation and edema of interstitium, indicating the onset of CRF development. Tubulo-interstitial nephritis and nephrosclerosis were dominated in untreated rats 16 weeks later. The use of RAAS drug blockade, as well as a comprehensive therapy with RAAS blockers and placental cryoextract stopped the inflammatory processes in renal tissue, restored blood circulation and normalized excretory function, which persisted for up to 16 weeks of observation.

Electron microscopic study of the membrane glycoproteins in the rat kidney after cisplatin treatment

1989 ◽  
Vol 47 ◽  
pp. 912-913
Author(s):  
S.K. Aggarwal
Keyword(s):  
Alkaline Phosphatase ◽  
Rat Kidney ◽  
Light And Electron Microscopy ◽  
Kidney Tissue ◽  
Membrane Glycoproteins ◽  
Electron Microscopic ◽  
Before And After ◽  
Interstrand Cross Links ◽  
Cross Links

The proposed primary mechanism of action of the anticancer drug cisplatin (Cis-DDP) is through its interaction with DNA, mostly through DNA intrastrand cross-links or DNA interstrand cross-links. DNA repair mechanisms can circumvent this arrest thus permitting replication and transcription to proceed. Various membrane transport enzymes have also been demonstrated to be effected by cisplatin. Glycoprotein alkaline phosphatase was looked at in the proximal tubule cells before and after cisplatin both in vivo and in vitro for its inactivation or its removal from the membrane using light and electron microscopy.Outbred male Swiss Webster (Crl: (WI) BR) rats weighing 150-250g were given ip injections of cisplatin (7mg/kg). Animals were killed on day 3 and day 5. Thick slices (20-50.um) of kidney tissue from treated and untreated animals were fixed in 1% buffered glutaraldehyde and 1% formaldehyde (0.05 M cacodylate buffer, pH 7.3) for 30 min at 4°C. Alkaline phosphatase activity and carbohydrates were demonstrated according to methods described earlier.

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