Inhibition of human placenta aldose reductase by tannic acid.

Sawada, Hideo; Hamatake, Michiko; Hara, Akira; Nakagawa, Makoto; Nakayama, Toshihiro

doi:10.1248/cpb.37.1662

Cited by 13 publications

(10 citation statements)

References 1 publication

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“…p < 0.05 and p < 0.01 were considered statistically significant. IC 50 (inhibitor concentration that produces 50% inhibition) was estimated using linear regression method of plots of the percent inhibitory activity against the concentration of the tested compounds using Microsoft Excel.…”

Section: Discussionmentioning

confidence: 99%

“…Flavonoids and related compounds are the most widely studied natural products family with aldose reductase inhibitory activity. [50,51] Polyphenolic extract of I. frutescens were assessed for inhibitory activity against lens aldose reductase isolated from Wistar albino rats. Polyphenolic extract significantly inhibits the aldose reductase activity in vitro and is primarily caused by the presence of phenolic compounds and flavonoids in PPE.…”

Section: Drug Treatmentmentioning

confidence: 99%

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Polyphenolic Extract ofIchnocarpus FrutescensAttenuates Diabetic Complications in Streptozotocin-Treated Diabetic Rats

Kumarappan

Mandal

2008

Renal Failure

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Diabetic nephropathy is one of the major complications of diabetes. Oxidative stress is implicated as an important mechanism by which diabetes causes nephropathy. The aim of the study was to examine the involvement of oxidative stress in the progression of nephropathy in STZ diabetic animals and to evaluate the potential of polyphenolic extract (PPE) in the treatment of diabetes mellitus. In this study, we examined whether prolonged oral administration of polyphenolic extract of Ichnocarpus frutescens could prevent the progress or improve the outcome of diabetic nephropathy induced by oxidative stress in STZ diabetic rats. Intraperitoneal glucose tolerance test (IPGTT) revealed a significant decrease in blood glucose levels at 180 min after glucose loading in Wistar albino rats fed with PPE. During the eight weeks of experimental period, diabetic rats exhibited wide range of symptoms, including loss of body weight, hyperglycemia, polyuria, proteinuria, renal enlargement, and total renal dysfunction. A significant increase in TBARS level was observed in diabetic kidney, which was accompanied by a significant decrease in enzymatic and non-enzymatic antioxidant levels. After eight weeks, PPE-treated groups showed a lower level of blood glucose compared with non-treated STZ diabetic rats. The increases in urinary albumin and protein after eight weeks of treatment were significantly inhibited by prolonged treatment with PPE. In addition, PPE attenuates the adverse effects on hepatic biomarkers. We found that PPE can effectively protect against aldose reductase activity and protein damage (albumin glycation), and showed that its action was mainly due to enriched polyphenolic content. Our results also showed that treatment with PPE normalized the increase in hyperalgesia (i.e., the response to thermal stimuli) associated with the induction of diabetes by STZ. PPE administration in diabetic rats clearly ameliorated diabetic complications, suggesting not only a natural antioxidant but also supportive therapy for the treatment of type II diabetes.

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Section: Discussionmentioning

confidence: 99%

Section: Drug Treatmentmentioning

confidence: 99%

Polyphenolic Extract ofIchnocarpus FrutescensAttenuates Diabetic Complications in Streptozotocin-Treated Diabetic Rats

Kumarappan

Mandal

2008

Renal Failure

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“…Tannins have been found to be inhibitors of several enzyme activities, such as the human aldose reductase (Sawada et al 1989), pig gastric H + , (K + )-ATPase (Murakami et al 1992), rat brain and liver FOF 1 -AT- Fig. 1 Lineweaver-Burk plot for the inhibition of 1-NA glucuronidation in rat liver microsomes by tannic acid.…”

Section: Resultsmentioning

confidence: 99%

Inhibition of UDP-glucuronosyltransferases in rat liver microsomes by natural mutagens and carcinogens

Grancharov

Engelberg

Naydenova

et al. 2001

Archives of Toxicology

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Eight toxic compounds of natural origin present in the human diet or used as drugs were tested as inhibitors of UDP-glucuronosyltransferase (UGT) activity in rat liver microsomes with 1-naphthol (1-NA), phenolphthalein (PPh) and 4-nitrophenol (4-NP) as substrates. Strong inhibitory effects were observed with tannic acid (tannin) and the antifungal drug griseofulvin (GF): at a concentration of 1 mM, the two compounds completely suppressed the glucuronidation of 1-NA and PPh, respectively. A concentration of 0.1 mM still proved to be highly inhibitory, and even at a concentration as low as 50 microM, tannin produced nearly 50% inhibition of 1-NA conjugation. The UGT isoforms converting 4-NP were less sensitive to the tested compounds (with the exception of GF). Kinetic studies with tannin revealed an uncompetitive type of inhibition toward 1-NA, with an apparent Ki value of 20 microM. The inhibition by GF was non-competitive with respect to PPh and was of a mixed type toward UDP-glucuronic acid, with apparent Ki values of 40 microM and 30 microM, respectively. Tannin and GF did not act as substrates for rat microsomal UGT.

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“…For example, compound 1 inhibits proteasomal chymotrypsin-like activity (IC 50 ϭ0.035 mM), 23) collagenase (effective at 7-37 mM), 24) aldose reductase (IC 50 ϭ0.070 mM), 25) and epidermal growth factor (EGF) receptor tyrosine kinase (IC 50 ϭ0.3 mM), 26) and induces tumor cell death (effective at 10-30 mM). 27,28) Compound 2 inhibits u-PA-catalyzed plasminogen activation (IC 50 ϭ5 mM) 29) and EGF receptor tyrosine kinase (IC 50 ϭ0.1 mM), 30) and induces tumor cell death (effective at 30-300 mM).…”

Section: Discussionmentioning

confidence: 99%

Inhibitors of Autoactivation of Plasma Hyaluronan-Binding Protein (Factor VII Activating Protease)

Yamamoto

Nishimura

Okada

et al. 2011

Biological & Pharmaceutical Bulletin

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Plasma hyaluronan-binding protein (PHBP), a serine protease that can activate coagulation factor VII and prourokinase, circulates in a single-chain form (pro-PHBP) and autoproteolytically converts to an active twochain form with the aid of an effector such as spermidine and heparin. It has been postulated that PHBP plays roles in regulating inflammation, vascular function, fibrosis and atherosclerosis. From the comprehensive screening of natural sources for inhibitors of spermidine-induced pro-PHBP autoactivation, we identified several compounds with a polyphenol feature. Of these inhibitors, tannic acid (IC 50 ‫020.0؍‬ m mM), delphinidin (IC 50 ‫970.0؍‬ m mM), hamamelitannin (IC 50 ‫91.0؍‬ m mM), (؊)-epicatechin gallate (IC 50 ‫42.0؍‬ m mM), and 3,5-di-O-caffeoylquinic acid (IC 50 ‫0.1؍‬ m mM) were potent and selective, and did not inhibit heparin-induced pro-PHBP autoactivation and the active form of PHBP at concentrations 100 times higher than the respective IC 50 values. From evaluation of the activities of related compounds, it has been suggested that a compound with multiple aromatic rings with plural phenolic hydroxyl substituents exhibits potent activity. The inhibitory actions of delphinidin, hamamelitannin, (؊)-epicatechin gallate and 3,5-di-O-caffeoylquinic acid were attenuated by catechol, a minimum polyphenol unit. Thus, it is likely that pro-PHBP binds these potent inhibitors through its site(s) that recognize a catechollike structure. Our results would facilitate understanding of the molecular mechanism of pro-PHBP autoactivation and rational design of a compound for suppressing unregulated pro-PHBP activation.

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Inhibition of human placenta aldose reductase by tannic acid.

Cited by 13 publications

References 1 publication

Polyphenolic Extract ofIchnocarpus FrutescensAttenuates Diabetic Complications in Streptozotocin-Treated Diabetic Rats

Polyphenolic Extract ofIchnocarpus FrutescensAttenuates Diabetic Complications in Streptozotocin-Treated Diabetic Rats

Inhibition of UDP-glucuronosyltransferases in rat liver microsomes by natural mutagens and carcinogens

Inhibitors of Autoactivation of Plasma Hyaluronan-Binding Protein (Factor VII Activating Protease)

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