No abstract

Paeoniflorin (PF), a monoterpene glucoside, is a primary bioactive component of paeony, the root extract of Paeonia lactiflora. We tested the antioxidant effects of PF and its ability to prevent lipopolysaccharide (LPS)-induced oxidative stress. We intraperitoneally administered PF (2.5, 5, or 10 mg/kg) to rats for 20 days. On day 21, we injected the rats with LPS 4 h before sacrifice and measured serum levels of glutamate oxaloacetate transaminase, glutamate pyruvate transaminase, lactate dehydrogenase as well as the levels of malondialdehyde, superoxide dismutase, catalase, and glutathione peroxidase in liver whole-cell homogenates and mitochondrial fractions. LPS treatment increased levels of glutamate oxaloacetate transaminase, glutamate pyruvate transaminase, lactate dehydrogenase, and malondialdehyde, but PF treatment blocked these increases. LPS treatment also decreased antioxidant levels of superoxide dismutase, catalase, and glutathione peroxidase, but PF blocked these decreases. PF also protected liver tissue, as shown by histopathology. These results suggest that PF can protect against LPS-induced liver inflammation.

Reactive oxygen species (ROS), which include hydrogen peroxide and other chemical forms known as free radicals, such as superoxide anion, hydroxyl, and peroxyl radicals, are produced as part of normal and essential biological processes.1) Diverse antioxidant systems, both enzymatic and nonenzymatic, operate to control excessive levels of ROS. 1)A cell is generally able to maintain an appropriate balance between oxidants and antioxidants under normal conditions. When this balance is perturbed and shifts toward oxidative stress, either by an increase in oxidants or by a decrease in antioxidants, the cell becomes more susceptible to injuries, such as inflammation, 2) ischemia/reperfusion damage, 2,3) diabetes, 4) and atherosclerosis. 5-7) The oxidative stress established by excessive free radical generation may induce a number of alterations of cell constituents, including inactivation of enzymes, generation of reactive nitrogen species, damage of nucleic acid bases and proteins, and peroxidation of membrane lipids.To protect against the damage caused by oxidative stress, cells have a number of antioxidant enzymes and repair activities, most of which are expressed at low levels during normal growth. In mammalian cells, ROS are normally scavenged by three major types of primary antioxidant enzymes: copper-, zinc-, and manganese-dependent superoxide dismutase (CuZn-SOD and Mn-SOD), catalase (CAT) and glutathione peroxidase (GPx). The SODs convert superoxide anion into hydrogen peroxide (H 2 O 2 ), while CAT and GPx degrade H 2 O 2 into water. Furthermore, GPx degrades H 2 O 2 that originates from the oxidation of polyunsaturated fatty acids (PUFAs) in the presence of reduced glutathione (GSH) which is a key component of the antioxidant defense system. 8) In addition, ovariectomy has been shown to cause an increase in peroxide production by the liver and brain.9,10) Estrogens have antioxidant properties and can inhibit lipid peroxidation in vitro, which might contribute directly to their neuroprotective effect, 11) and the antioxidant metabolism of estrogen protection has been suggested to be independent of receptor binding. 12,13) Estrogen is an antioxidant and is capable of both reducing lipoprotein oxidation and decreasing artery wall production of superoxide anion.14-17) Women undergo natural menopause, called the primary event of the aging process, in their 40-50s. Estrogen declines precipitously in postmenopause. This ovarian hormone deficiency increases the generation of ROS. The excessive ROS induces oxidative stress that results in cell damage or death. Age-related increases in serum and tissue lipid peroxides have been demonstrated in rodents, 18) and increased levels of serum lipid peroxides have been found in elderly humans. 19)Salicornia herbacea (SH) is an annual herb growing in salt marshes and on muddy seashores. In Oriental medicine, SH has been used to treat a variety of conditions such as constipation, obesity, diabetes, asthma, arthritis, and cancer. 21) This plant has previously been shown to stim...

Oxidative stress due to reactive oxygen species (ROS) can cause oxidative damage to cells. Cells have a number of defense mechanisms to protect themselves from the toxicity of ROS. Mitochondria are especially important in the oxidative stress as ROS have been found to be constantly generated as an endogen threat. Mitochondrial defense depends mainly on superoxide dismutase (SOD) and glutathione peroxidase (GPx), whereas microsomal defense depends on catalase (CAT), which is an enzyme abundant in microsomes. SOD removes superoxide anions by converting them to H2O2, which can be rapidly converted to water by CAT and GPx. Also, GPx converts hydroperoxide (ROOH) into oxidized-glutathione (GSSG). Ovariectomized (OVX) rats are used as an oxidative stress model. An ovariectomy increased the levels of MDA, one of the end-products in the lipid peroxidative process, and decreased levels of the antioxidative enzymes; SOD, CAT and GPx. However, Chondroitin sulfate (CS) decreased the levels of MDA, but increased the levels of SOD, CAT and GPx in a dose-dependent manner. Moreover, inflammation and cirrhosis of liver tissue in CS- treated rats were significantly decreased. These results suggest that CS might be a potential candidate as an antioxidative reagent.