Cytoprotective Effect of Curcumin in Human Proximal Tubule Epithelial Cells Exposed to Shiga Toxin

Sood, Arpana; Mathew, Roy; Trachtman, Howard

doi:10.1006/bbrc.2001.4749

Cited by 35 publications

(21 citation statements)

References 24 publications

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“…time period, indicating the enhancement or at least maintenance of the effect of LPS; thus curcumin might only be effective on the early stage but become less powerful as incubation time increases. As a matter of fact, we did find a significant inhibition effect of 50 mM curcumin prior to 12 h. Finally, despite its cytoprotective effect, 26) curcumin was recently found to be cytotoxic against HK-2 cells at 50 mM. 27) Although no clear evidence supported the possible positive effect of curcumin on the synthesis, sorting and secretion of these two proteins, the relatively higher concentration of curcumin used herein should be considered when explaining these results.…”

Section: Effects Of Curcumin On the Secretion Of Il-8 In Lps-mentioning

confidence: 60%

Curcumin Attenuates Lipopolysaccharide-Induced Renal Inflammation

Zhong

Chen

Lin

et al. 2011

Biological & Pharmaceutical Bulletin

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Curcumin is a bright yellow compound found in turmeric, which is derived from the rhizomes of the plant Curcuma longa LINN, a perennial herb of the Zingerberaceae family. 1) It has been used for millennia as a wound-healing agent and for treating a large number of diseases in traditional Chinese and Indian medicine.2) A wide variety of cellular properties of curcumin have been demonstrated, including anti-inflammatory, antioxidant, antiproliferative, pro-apoptotic, anti-bacterial and anti-cancer activities.3) Among all these biological activities, the anti-inflammatory effects of curcumin have been assessed in various in vitro systems and in experimental animal systems. 4,5) Renal inflammation is the main pathological change in many acute and chronic kidney diseases. Several studies have demonstrated that curcumin played a positive role in inflammation-related renal injury using various animal models, 6-10) of which only one study used cultured cell lines as the in vitro model. 10) Lipopolysaccharide (LPS), the product of Gram-negative bacteria, is an important inflammatory factor and has been widely used to induce renal inflammation models when studying inflammation-related renal diseases. [11][12][13] This model was also employed in the present study to investigate the effect of curcumin on renal inflammation. In a variety of acute and chronic renal inflammation, renal tubular epithelial cells were not only the victims, but also actively participate in the process of glomerular sclerosis and renal fibrosis by secreting a variety of inflammatory chemokines and extracellular matrix. Considering the important role renal tubular epithelial cells played in renal inflammation, a human proximal tubule cell line (HK-2 cells) was selected as the in vitro model. By using both in vitro and in vivo models, we attempted to obtain an allaround evaluation of curcumin on renal inflammation, and also gain a preliminary view of the underlying mechanism. MATERIALS AND METHODSChemicals Keratinocyte-serum-free medium (SFM) cell culture medium, fetal bovine serum, trypsin, and Trizol RNA extraction reagent were purchased from Gibco Life Technologies, Inc. .).Cell Culture HK-2 cells, an immortalized proximal tubular epithelial cell (PTEC) line from normal adult human kidney, were obtained from the American Type Culture Collection (Manassas, VA, U.S.A.). HK-2 cells were cultured in Keratinocyte-SFM cell culture medium containing 2% fetal calf serum at 37°C and 5% CO 2 .Animals Kunming mice of specific pathogen free (SPF) level (6-8 weeks old), ranging from 18 to 22 g, were purchased from the Laboratory Animal Center of Shanghai Jiao Tong University (Shanghai, China). The animals were maintained under climate-controlled conditions with a 12-h light/dark cycle, and were fed standard rodent chow and water. The guidelines for the care of the animals were strictly The present study demonstrated that curcumin has a protective effect on LPS-induced experimental renal inflammation, and this effect might be attributed to its inhibitory effec...

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Section: Effects Of Curcumin On the Secretion Of Il-8 In Lps-mentioning

confidence: 60%

Curcumin Attenuates Lipopolysaccharide-Induced Renal Inflammation

Zhong

Chen

Lin

et al. 2011

Biological & Pharmaceutical Bulletin

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“…Curcumin also directly blocks the I/R-mediated increase in JNK1 and c-Jun, thus decreasing I/R-induced cell death and apoptosis [22] . It was reported that curcumin, a potent stimulator of stress-induced Hsp70 expression, exhibits protective effects against some forms of stress, such as heat or toxicant by mechanisms distinct from the increased hepatic Hsp70 expression [23][24][25] . In this study, we explored whether curcumin pretreatment could increase the expression of Hsp70 in rat livers after warm I/R.…”

Section: Discussionmentioning

confidence: 99%

Protective effect of curcumin against liver warm ischemia/reperfusion injury in rat model is associated with regulation of heat shock protein and antioxidant enzymes

Shen

Zhang²,

Xiang³

et al. 2007

WJG

138

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but had no effect on the level of endothelial NO synthase (eNOS) after reperfusion in liver. The 7 d survival rate was significantly higher in C + I/R group than in I/R group. CONCLUSION:Curcumin has protective effects against hepatic I/R injury. Its mechanism might be related to the overexpression of Hsp70 and antioxidant enzymes. Abstract AIM: To investigate the hypothesis that the protective effects of curcumin in hepatic warm ischemia/reperfusion (I/R) injury are associated with increasing heat shock protein 70 (Hsp70) expression and antioxidant enzyme activity. METHODS:Sixty Sprague-Dawley male rats were randomly divided into sham, I/R, C + I/R groups. The model of reduced-size liver warm ischemia and reperfusion was used. Curcumin (50 mg/kg) was administered by injection through a branch of superior mesenteric vein at 30 min before ischemia in C + I/R group. Five rats were used to investigate the survival during 1 wk after operation in each group. Blood samples and liver tissues were obtained in the remaining animals after 3, 12, and 24 h of reperfusion to assess serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), liver tissue NO2 -+ NO3 -, malondialdehyde (MDA) content, superoxide dismutase (SOD), catalase (CAT), nitricoxide synthase (NOS) and myeloperoxidase (MPO) activity, Hsp70 expression and apoptosis ratio. RESULTS:C o m p a r e d w i t h I / R g r o u p , c u r c u m i n pretreatment group showed less ischemia/reperfusioninduced injury. CAT and SOD activity and Hsp70 expression increased significantly. A higher rate of apoptosis was observed in I/R group than in C + I/R group, and a significant increase of MDA, NO2 -+ NO3 -and MPO level in liver tissues and serum transaminase concentration was also observed in I/R group compared to C + I/R group. Curcumin also decreased the activity of inducible NO synthase (iNOS) in liver after reperfusion,

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“…Extensive studies have utilized HK-2 cells to study in vitro renal physiology and pathology [16, 17, 18, 19]. Moreover, HK-2 cells have been studied as an in vitro model of renal apoptosis induction with multiple stimuli including oxidative stress [20], Shiga toxin [21]and sustained hypo-osmotic stress [22]. …”

Section: Discussionmentioning

confidence: 99%

Local Anesthetics Induce Human Renal Cell Apoptosis

Lee¹,

Xu²,

Siegel³

et al. 2003

Am J Nephrol

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Renal cell apoptosis contributes significantly to the pathogenesis of acute renal failure. Local anesthetics induce apoptosis in neuronal and lymphocytic cell lines. We examined the effects of chronic (48 h) local anesthetic treatment (lidocaine, bupivacaine and tetracaine) on human proximal tubular (HK-2) cells. Apoptosis induction was assessed by detecting poly(ADP)-ribose polymerase fragmentation, caspase activation, terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling (TUNEL) staining, DNA laddering and by cellular morphology. Cell death was quantified by measuring neutral red dye uptake and lactate dehydrogenase released into the cell culture medium. All 3 local anesthetics caused concentration-dependent cell death, induced HK-2 cell apoptosis and potentiated TNF-α induced apoptosis. Local anesthetics induced HK-2 cell apoptosis by activation of caspases 3, 6, 7, 8 and 9. ZVAD-fmk, a pan-caspase inhibitor, blocked the local anesthetic induced HK-2 cell apoptosis. Local anesthetics also inhibited the activities of anti-apoptotic kinases protein kinase B (Akt) and extracellular signal regulated mitrogen-activated protein kinase. Local anesthetic’s pro-apoptotic effects are independent of sodium channel inhibition as tetrodotoxin, a selective voltage-gated sodium channel blocker, failed to mimic local anesthetic-mediated induction or potentiation of HK-2 cell apoptosis. We conclude that local anesthetics induce human renal cell apoptotic signaling by caspase activation and via inhibition of pro-survival signaling pathways.

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Cytoprotective Effect of Curcumin in Human Proximal Tubule Epithelial Cells Exposed to Shiga Toxin

Cited by 35 publications

References 24 publications

Curcumin Attenuates Lipopolysaccharide-Induced Renal Inflammation

Curcumin Attenuates Lipopolysaccharide-Induced Renal Inflammation

Protective effect of curcumin against liver warm ischemia/reperfusion injury in rat model is associated with regulation of heat shock protein and antioxidant enzymes

Local Anesthetics Induce Human Renal Cell Apoptosis

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