2-2--azino-di-(3-ethylbenzothiazoline)-6-sulfonic-acid and pyrogallol-sulfonphthalein

In the current study, we compared purified Salvia miltiorrhiza extract (PSME) with Angiotensin-converting enzyme inhibitor, Ramipril, in in vitro experiments and also in vivo using animal model of myocardial infarction. PSME was found to have a significantly higher trolox equivalent antioxidant capacity which indicated a great capacity for scavenging free radicals. PSME could also prevent pyrogallo red bleaching and DNA damage. After 2 weeks treatment with PSME or Ramipril, survival rates of rats with experimental myocardial infarction were marginally increased (68.2% and 71.4%) compared with saline (61.5%). The ratios of infarct size to left ventricular size in both PSME-and Ramipril-treated rats were significantly less than that in the saline-treated group. Activity of cardiac antioxidant enzyme superoxide dismutase (SOD) was significant higher while level of Thiobarbituric acid-reactive substances (TBARs) was lower in the PSME treated group. Purified and standardized Chinese herb could provide an alternative regimen for the prevention of ischemic heart disease.

Topics: Analysis of Variance; Animals; Antioxidants; Benzothiazoles; DNA Damage; Drugs, Chinese Herbal; Gas Chromatography-Mass Spectrometry; Male; Myocardial Infarction; Myocardial Ischemia; Phytotherapy; Pyrogallol; Ramipril; Rats; Rats, Wistar; Salvia miltiorrhiza; Spectrophotometry; Sulfonic Acids; Superoxide Dismutase; Thiobarbituric Acid Reactive Substances; Ventricular Remodeling

Peroxynitrite is implicated in numerous human diseases. Hence, there is considerable interest in potential therapeutic peroxynitrite scavengers. It has been claimed that uric acid is a powerful peroxynitrite scavenger. We previously observed that uric acid is a powerful inhibitor of tyrosine nitration induced by peroxynitrite, but fails to prevent alpha(1)-antiproteinase (alpha(1)-AP) inactivation induced by peroxynitrite. However, the reactivity of peroxynitrite is significantly modified by bicarbonate and this has not been considered in evaluating the scavenging activity of uric acid and other endogenous antioxidant compounds. In the presence of bicarbonate (25 mM), the ability of uric acid, ascorbate, Trolox, and GSH to inhibit peroxynitrite-mediated tyrosine and guanine nitration is decreased. Protection against peroxynitrite-mediated alpha(1)-AP inactivation is also decreased by ascorbate, Trolox, and GSH, but it is enhanced by uric acid. Bicarbonate also inhibits the ability of these compounds to prevent peroxynitrite-mediated ABTS radical cation formation. However, the abilities of these antioxidants to prevent peroxynitrite-mediated bleaching of pyrogallol red are enhanced by bicarbonate. These results show that physiologic concentrations of bicarbonate substantially modify the ability of uric acid to prevent peroxynitrite-mediated reactions. This study highlights the need to use several different assays in the presence of physiologically relevant concentrations of bicarbonate when assessing compounds for peroxynitrite scavenging, in order to avoid misleading results.

Topics: alpha 1-Antitrypsin; Antioxidants; Ascorbic Acid; Benzothiazoles; Bicarbonates; Chromans; Coloring Agents; Glutathione; Guanine; Humans; Indicators and Reagents; Peroxynitrous Acid; Pyrogallol; Reactive Nitrogen Species; Serine Proteinase Inhibitors; Sulfonic Acids; Tyrosine; Uric Acid