Inhibitory effect of hot-water extract from dried fruit of Crataegus pinnatifida on low-density lipoprotein (LDL) oxidation in cell and cell-free systems.

The dried fruit of Crataegus pinnatifida, a local soft drink material and medical herb, was found to possess potential against oxidative stress. In the preliminary study, the antioxidant potential of a hot-water extract obtained from the dried fruit of C. pinnatifida (CF-H) was evaluated in terms of its capacity of quenching 1,1-diphenyl-2-picrylhydrazyl free radicals (EC(50) = 0.118 mg/mL). After content analysis, it was found that CF-H is mainly composed of polyphenols including flavonoids (6.9%), procyanidins (2.2%), (+)-catechin (0.5%), and (-)-epicatechin (0.2%). The antioxidative bioactivity of CF-H had been assess previously using the models of CuSO(4) as cell-free system and sodium nitroprusside (SNP) plus macrophage RAW 264.7 cells as cell system to induce human low-density lipoprotein oxidation. CF-H was found to inhibit relative electrophoretic mobility and thiobarbituric acid reactive substances at the concentration of 0.5-1.0 mg/mL in the cell-free system and at 0.01-0.10 mg/mL in the cell system. Furthermore, it was found that CF-H decreased the SNP-induced cell lipid peroxidation and reduced glutathione depletion.

Induction of apoptosis by penta-acetyl geniposide in rat C6 glioma cells.

Penta-acetyl geniposide, (Ac)(5)-GP, was produced by acetylation of a glycoside, isolated from an extract of Gardenia fructus. Previously, we have reported that C6 glioma cells could be inhibited in culturing as well as in bearing rats by treating with (Ac)(5)-GP. In this study, the effect and action of (Ac)(5)-GP on inducing cell death was examined in rat C6 glioma cells. Treatment of C6 glioma cells with (Ac)(5)-GP caused cell death, chromatin condensation, and internucleosomal DNA ladder. Also, cell cycle arrest at G(0)/G(1) phase revealed that (Ac)(5)-GP-induced cell death appears to be mediated by apoptosis. In addition, the results also showed that p53 and c-Myc increased due to treatment of (Ac)(5)-GP in a dose-response and time-dependent manner. Concomitant with the expression of p53 and c-Myc, decreased level of Bcl-2 and increased level of Bax protein were observed. These results suggest that cell death caused by (Ac)(5)-GP through apoptosis and cell cycle arrest at G(0)/G(1) may be associated with the induction of p53, c-Myc and may be mediated with apoptosis-related Bcl-2 family proteins.

Induction of epidermal proliferation and expressions of PKC and NF-kappaB by betel quid extracts in mouse: the role of lime-piper additives in betel quid.

Components of betel quid (BQ) have been investigated for genotoxicity, mutagenicity, and animal toxicity. However, little information exists regarding their carcinogenic characteristics. Considerable attention has already been focused on tumor promoters that occur environmentally for human uptake. In this study, the promoting effects of BQ and lime-piper additives (LPA) in BQ on epidermal hyperplasia in CD-1 mouse skin are investigated. In the present study, we found that BQ and LPA at concentrations of 25,50,75 mg/ml caused significant induction of hyperplasia, but only LPA caused an increase of epidermal ornithine decarboxylase (ODC). Treatment of mouse skin with LPA caused remarkable increases in the production of H(2)O(2) by 2.41-, 3.90-, and 3.76-fold (for the above-indicated concentrations respectively); as well as marked increases of myeloperoxidase (MPO) by 1.43-, 2.70-, and 2.29-fold. Application of LPA or BQ (50,100,150 mg/ml) also caused induction of protein kinase C-alpha (PKC-alpha) and NF-kappaB. LPA exhibited more significant effect than BQ. Thus, LPA might make a major contribution to the BQ-induced expression of PKC and NF-kappaB. These results indicated that BQ has the potential of being promoting agents, and that LPA should play a major role in increasing the effects of BQ-caused skin hyperplasia and inflammation. The promoting effects of BQ and LPA on mouse skin were associated with the induction of the expressions of PKC and NF-kappaB.

Hibiscus protocatechuic acid or esculetin can inhibit oxidative LDL induced by either copper ion or nitric oxide donor.

Oxidation of low-density lipoprotein (LDL) could increase the incidence of atherosclerosis. Previous studies have shown that copper and sodium nitroprusside (SNP) possess the ability to oxidize LDL in a dose-dependent condition. They increase the existing negative charge in LDL and increase the electrophoretic mobility. In this study, we used protocatechuic acid (PCA) and/or esculetin (ECT) to define the antioxidative activity in oxidative LDL by relative electrophoretic mobility (REM) and thiobarbituric acid-relative substances (TBARS). The data showed that ECT and PCA possessed stronger antioxidative activity than vitamin E in oxidative LDL. A previous study showed that the level of oxidative LDL can be determined by the cholesterol degradation and fragmentation of Apo B. Our results showed that Cu(2+)-mediated oxidative LDL can induce 31% cholesterol degradation and significant fragmentation of Apo B. Both PCA and ECT exhibited remarkable ability to rescue the cholesterol degradation and Apo B fragmentation. Taken together, both PCA and ECT showed strong potency to inhibit oxidative LDL induced by copper or an NO donor. Additionally, their nontoxic characteristics elevated the possibility for their use in the daily diet; and should further prevent atherosclerosis effectively.