Search

The purpose of this study was to evaluate the effects of Baduanjin exercise on oxidative stress, antioxidant status and quality of life in middle-aged women. A quasi-experimental design was adopted. Subjects were 31 middle-aged women. Subjects completed a supervised and standardized Baduanjin exercise program 3 times a week for 12 weeks. Malondialdehyde (MDA) level was measured and determined by using a spectrophotometer for oxidative stress. The superoxide dismutase (SOD) was measured for the antioxidant status. A 36-item Short Form Health Survey (SF-36) was used to evaluate changes in quality of life. All outcome measures were collected before intervention and at the end of a 12-week intervention. The results suggest that there are significant differences in serum SOD level with Baduanjin exercise. SOD level was significantly increased after exercise ( p < 0.05). Baduanjin exercise contributed significantly to antioxidant status on these samples. However, a reduction in MDA level was observed. The t-test value was 2.03 with a p-value of 0.052. The changes may be meaningful at a 5% level. There are significant improvements in quality of life after the exercise program. Subjects had greater improvements in 4 dimensions of SF-36, namely physical function, body pain, social function and general mental health ( p < 0.05). In conclusion, Baduanjin exercise has beneficial effects on improving quality of life, increasing antioxidant enzymes and reducing oxidative stress in middle-aged women. Reduction of MDA level may be more attributable to the increase in the antioxidant enzyme SOD.

Angelica archangelica (AAA) has been effectively used in folk medicines as a remedy against stomachal and intestinal disturbances, arthritic disease, etc. However, there is still lack of scientific proof about its antioxidant capability. This study aimed at investigating the effects of total AAA against chronic ethanol-induced hepatotoxicity. ICR mice were divided into five groups, each consisting of 10 animals. A single dose of ethanol (70%, 0.1 ml, p.o.) was used to induce hepatotoxicity in these mice which resulted in a significant elevation of the activities of serum GOT and GPT. Treatment of mice with AAA (10, 25, and 50 mg/kg p.o.) after 2 weeks ameliorated the ethanol-induced hepatotoxicity effects. Hepatotoxicity was evidenced by a significant increase in hepatic lipid peroxidation manifested as the presence of malondialdehyde. It was found that AAA inhibits the malondialdehyde formation in mouse liver homogenates both in vitro and in vivo. AAA is cytoprotective agent effective against chronic ethanol-induced hepatotoxicity, possibly through inhibition of the production of oxygen free radicals that cause lipid peroxidation, and hence indirectly protects the liver from oxidative stress.

The hot water extract of the mushroom Ganoderma lucidum was shown to have antioxidative effect against heart toxicity. Investigations into the mechanisms of action, level of lipid peroxidation level in vivo, and superoxide scavenging activity were also conducted. The mice were divided into six groups with ten animals in each group. Ganoderma lucidum, at doses of 10, 25 and 50 mg/kg (p.o.) was administered. Superoxide anions were assayed by UV spectrophotometer using the cytochrome C reduction method. The results of this study showed that Ganoderma lucidum exhibited a dose-dependent antioxidative effect on lipid peroxidation and superoxide scavenging activity in mouse heart homogenate. Additionally, this result indicated that heart damage induced by ethanol shows a higher malonic dialdehyde level compared with heart homogenate treated with Ganoderma lucidum. It is concluded that the antioxidative activity may therefore contribute to the cardioprotective effect of Ganoderma lucidum, and may therefore protect the heart from superoxide induced damage.

The purpose of this study was to investigate the antioxidant effects of a hot water extract of Panax notoginseng (PNG) against chronic ethanol-induced hepatotoxicity. Fifty mice were divided into five equal groups with 10 in each group. Group 1 (control) received saline, whereas group 2 received ethanol (70%, 0.1 mL, p.o.) once daily for 4 weeks, which induced hepatotoxicity, manifested biochemically by a significant elevation of serum enzyme activities, such as SGOT and SGPT. Hepatotoxicity was further evidenced by a significant increase in the hepatic lipid peroxidation measured. Groups 3–5 were administered a hot water extract of PNG at doses of 10, 25 and 50 mg/kg 2 weeks after initiating oral administration of ethanol, for a further 2 weeks. PNG ameliorated the rise in serum sGOT and sGPT induced by chronic ethanol administration. The mice were killed after PNG administration. In a separate study, PNG inhibited the lipid peroxidation in the mouse liver homogenate induced by ethanol in a dose-dependent manner. The findings indicate that PNG is an efficient cytoprotective agent against chronic ethanol-induced hepatotoxicity, possibly through inhibition of the production of oxygen-free radicals that cause lipid peroxidation. Copyright © 2003 John Wiley & Sons, Ltd.

Acute p.o. administration of absolute ethanol (1.0 ml/kg) to fasted rats produced extensive necrosis of gastric mucosa. Pretreatment with p.o. administration of propolis ethanol extract (PEE) could effectively and dose-dependently prevent such necrosis. This protective effect is called "cytoprotection." The maximal cytoprotective effect against absolute ethanol (AE)-induced gastric mucosal lesion was observed 1 hour after PEE administration. A gross examination of the gastric mucosa showed a marked improvement in groups receiving PEE. In order to further investigate the gastric protective mechanism of PEE, lipid peroxidation (LPO) levels in vivo and in vitro were estimated. PEE exhibited dose-dependent superoxide scavenging activity and antioxidant effects on AE-induced LPO in rat gastric mucosal homogenates. It was concluded that the gastric protective mechanism of PEE was due, at least in part, to its ability to inhibit LPO, and hence indirectly protect the gastric mucosa from oxidative stress.

2,3,5,6-Tetramethylpyrazine (TMP) is well known as a true calcium antagonist. The aim of this study was to investigate the hepatoprotective and therapeutic effects of TMP on acute econazole-induced liver injury. The hepatological effect of various concentrations of TMP was first assessed by the biochemical assays of SGOT and SGPT and then by hepatohistological microscopic examination. The dose-response relationship of liver injury induced by various doses of econazole was observed simultaneously from serum biochemical assay of SGOT and SGPT, and also from hepatohistological microscopic examination, by determination of the hepatoprotective effects of various concentrations of TMP on SGOT and SGPT elevation induced by a hepatotoxic dose of econazole (300 mg/kg). The inhibitory effect of various concentrations of TMP or vitamin E (positive control, 0.5 mM in vitro, 0.69 mM in vivo) on FeCl 2 -induced (in vitro) or econazole-induced (in vivo) lipid peroxidation was also investigated. The superoxide scavenging activity of various concentrations of TMP in econazole-damaged rat liver homogenate was assessed by the cytochrome C reduction method. Results showed that the hepatoprotective effect of TMP might be, at least in part, due to its inhibitory ability on membrane lipid peroxidation and free radical formation, or due to its free radical scavenging ability. Improvement of serum transaminases and MDA levels in rat liver homogenate, hepatohistological microscopic examination, and assessment of free radical scavenging activity by the cytochrome C reduction method were used to detect hepatoprotective and therapeutic effects of TMP on acute econazole-induced liver injury.