Effect of green tea extract on cardiac hypertrophy following 5/6 nephrectomy in the rat

Priyadarshi, Snigdha; Valentine, Brandon; Han, Chi Dong; Федорова, О. В.; Bagrov, Alexei Y.; Liu, Jiang; Periyasamy, Sumudra; Kennedy, David J.; Malhotra, Deepak; Xie, Zijian; Shapiro, Joseph I.

doi:10.1046/j.1523-1755.2003.00914.x

Cited by 67 publications

(55 citation statements)

References 20 publications

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“…Immunization against MBG-BSA in partial nephrectomy animals was associated with a decrease in U MBG V compared with partial nephrectomy alone. Neither plasma or urine OLC levels were different between sham and partial nephrectomy as we have reported previously 11 nor did we see a significant effect of either MBG supplementation or immunization against MBG on plasma or urine OLC levels (Table 1).…”

Section: Changes In Mbg and Other Hormonescontrasting

confidence: 42%

“…13,14 Cardiotonic steroid signaling through the sodium pump causes well-described changes in gene expression, which can be blocked by antioxidants. 11,18,19 The purpose of the current study was to examine whether this signaling by cardiotonic steroids through the Na/K- ATPase, which has been extensively characterized in vitro, actually plays a significant role in an in vivo model of uremic cardiomyopathy. Our observations can be summarized as follows.…”

Section: Discussionmentioning

confidence: 99%

“…8,9 Elevations of circulating MBG have been clearly demonstrated in both clinical and experimental renal failure, whereas another cardiotonic steroid, endogenous ouabain, does not increase at 4 weeks in experimental renal failure. 10,11 Interestingly, investigators postulated a role for endogenous natriuretic substances in the pathobiology of uremia decades before their identification. 12 Our group and others have observed that cardiotonic steroids induce signaling through the plasmalemmal Na/K-ATPase, which resides in caveolae.…”

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confidence: 99%

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Central Role for the Cardiotonic Steroid Marinobufagenin in the Pathogenesis of Experimental Uremic Cardiomyopathy

et al. 2006

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Abstract-Patients with chronic renal failure develop a "uremic" cardiomyopathy characterized by diastolic dysfunction, cardiac hypertrophy, and systemic oxidant stress. Patients with chronic renal failure are also known to have increases in the circulating concentrations of the cardiotonic steroid marinobufagenin (MBG). On this background, we hypothesized that elevations in circulating MBG may be involved in the cardiomyopathy. First, we observed that administration of MBG (10 g/kg per day) for 4 weeks caused comparable increases in plasma MBG as partial nephrectomy at 4 weeks. MBG infusion caused increases in conscious blood pressure, cardiac weight, and the time constant for left ventricular relaxation similar to partial nephrectomy. Decreases in the expression of the cardiac sarcoplasmic reticulum ATPase, cardiac fibrosis, and systemic oxidant stress were observed with both MBG infusion and partial nephrectomy. Next, rats were actively immunized against a MBG-BSA conjugate or BSA control, and partial nephrectomy was subsequently performed. Immunization against MBG attenuated the cardiac hypertrophy, impairment of diastolic function, cardiac fibrosis, and systemic oxidant stress seen with partial nephrectomy without a significant effect on conscious blood pressure. These data suggest that the increased concentrations of MBG are important in the cardiac disease and oxidant stress state seen with renal failure.

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Section: Changes In Mbg and Other Hormonescontrasting

confidence: 42%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Central Role for the Cardiotonic Steroid Marinobufagenin in the Pathogenesis of Experimental Uremic Cardiomyopathy

et al. 2006

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“…Further evidence for this phenomenon being dependent on signaling through the Na/ K-ATPase was that this increase was prevented by reactive oxygen species scavenging, antagonism, or knockout of Src, as well as prevention of EGFR transactivation, maneuvers that we have demonstrated previously to block signal transduction through the Na/K-ATPase signalsome. 13,14,[22][23][24] We also observed that the increases in collagen production were associated with increases in proline incorporation, as well as increases in mRNA for collagen-1. No increase in procollagen-1 stability could be demonstrated in response to MBG.…”

Section: Discussionmentioning

confidence: 96%

Marinobufagenin Stimulates Fibroblast Collagen Production and Causes Fibrosis in Experimental Uremic Cardiomyopathy

et al. 2007

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Abstract-We have observed recently that experimental renal failure in the rat is accompanied by increases in circulating concentrations of the cardiotonic steroid, marinobufagenin (MBG), and substantial cardiac fibrosis. We performed the following studies to examine whether MBG might directly stimulate cardiac fibroblast collagen production. In vivo studies were performed using the 5/6th nephrectomy model of experimental renal failure (PNx), MBG infusion (MBG), PNx after immunization against MBG, and concomitant PNx and adrenalectomy. Physiological measurements with a Millar catheter and immunohistochemistry were performed. In vitro studies were then pursued with cultured isolated cardiac fibroblasts. We observed that PNx and MBG increased MBG levels, blood pressure, heart size, impaired diastolic function, and caused cardiac fibrosis. PNx after immunization against MBG and concomitant PNx and adrenalectomy had similar blood pressure as PNx but less cardiac hypertrophy, diastolic dysfunction, and cardiac fibrosis. MBG induced increases in procollagen-1 expression by cultured cardiac fibroblasts at 1 nM concentration. These increases in procollagen expression were accompanied by increases in collagen translation and increases in procollagen-1 mRNA without any demonstrable increase in procollagen-1 protein stability. The stimulation of fibroblasts with MBG could be prevented by administration of inhibitors of tyrosine phosphorylation, Src activation, epidermal growth factor receptor transactivation, and N-acetyl cysteine. Based on these findings, we propose that MBG directly induces increases in collagen expression by fibroblasts, and we suggest that this may be important in the cardiac fibrosis seen with experimental renal failure. (Hypertension. 2007;49:215-224.)

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“…Plant steroids have been thoroughly described for their pharmacological properties, including hypocholesterolemic (1), antidiabetic (2) and antioxidant activities (3,4). Particular attention has been given to their potential for cancer chemoprevention, especially as apoptosis inducers (5)(6)(7)(8)(9)(10).…”

Section: Introductionmentioning

confidence: 99%

Inhibition of human rheumatoid arthritis synovial cell survival by hecogenin and tigogenin is associated with increased apoptosis, p38 mitogen-activated protein kinase activity and upregulation of cyclooxygenase-2

Liagre¹,

Vergne-Salle²,

Léger³

et al. 2007

Int J Mol Med

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Abstract. We conducted our study to assess the antiproliferative and proapoptotic potential of hecogenin and tigogenin, two saponins which are structurally similar to diosgenin. We particularly focused our attention on mitogenactivated protein kinase (MAPK) activation in relation to apoptosis but also with the COX-2 expression and activity. Rheumatoid arthritis (RA) synoviocytes were isolated from fresh synovial biopsies obtained from five RA patients undergoing hip arthroplasty. Measurement of cell proliferation was determined using the MTT assay. Apoptosis was evaluated by studying caspase-8, caspase-9 and caspase-3 activities but also by quantification of DNA fragmentation. Quantification of human phospho-MAPKs was realized by ELISA. COX-2 expression was demonstrated by Western blot analysis and COX-2 activity by assay of endogenous prostaglandin E 2 (PGE 2 ) production. Tigogenin was more effective than hecogenin in inducing apoptosis in human RA fibroblast-like synoviocytes (FLS) which was caspase dependent but poly(ADP-ribose) polymerase independent and characterized by DNA fragmentation. Our results demonstrated hecogenin-and tigogenin-induced apoptosis through activation of p38 without affecting the JNK and ERK pathways. Indeed, pretreatment with a p38 inhibitor decreased saponin-induced apoptosis with a significant decrease in DNA fragmentation. Furthermore, the rate of apoptosis induced by hecogenin or tigogenin was associated with overexpression of COX-2 correlated with overproduction of endogenous PGE 2 . These new results provide strong evidence that a family of structurally similar plant steroids is capable of inducing apoptosis in human RA FLS with different rates and different signalling pathways. This study also confirms the discussed appearance of the downregulation or upregulation of COX-2 in cell apoptosis as a function of cell type. IntroductionPlant steroids have been thoroughly described for their pharmacological properties, including hypocholesterolemic (1), antidiabetic (2) and antioxidant activities (3,4). Particular attention has been given to their potential for cancer chemoprevention, especially as apoptosis inducers (5-10).Apoptosis is considered to be one of the mechanisms regulating autoimmune diseases such as rheumatoid arthritis (RA) (11). In the pathogenesis of RA, it is thought that the normal balance between proliferation and apoptosis of synovial fibroblasts is lost, leading to hyperplasia of these fibroblasts (12). Activated synovial cells cause growth of synovium in the articular cavity along with angiogenesis, invade the adjacent bone, promote production of inflammatory mediators by inflammatory cells, and cause cartilage and bone destruction (13). Therefore, it has been shown that stimulation of apoptosis in synovial fibroblasts might be useful for the treatment of RA (14,15).We showed for the first time that a plant steroid, diosgenin, inhibited the growth of human RA fibroblast-like synoviocytes (FLS) with apoptosis induction characterized by a loss of mitochondrial me...

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Effect of green tea extract on cardiac hypertrophy following 5/6 nephrectomy in the rat

Cited by 67 publications

References 20 publications

Central Role for the Cardiotonic Steroid Marinobufagenin in the Pathogenesis of Experimental Uremic Cardiomyopathy

Central Role for the Cardiotonic Steroid Marinobufagenin in the Pathogenesis of Experimental Uremic Cardiomyopathy

Marinobufagenin Stimulates Fibroblast Collagen Production and Causes Fibrosis in Experimental Uremic Cardiomyopathy

Inhibition of human rheumatoid arthritis synovial cell survival by hecogenin and tigogenin is associated with increased apoptosis, p38 mitogen-activated protein kinase activity and upregulation of cyclooxygenase-2

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