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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.

The study objective of this research is in order to investigate the hepatoprotective and therapeutic effects of propolis ethanol extract (PEE) on acute econazole-induced liver injury. Positive control of various concentrations of PEE on liver function and the dose-response relationship of liver injury induced by various doses of econazole were firstly observed from biochemical assay of serum level of aspartate transaminase (SGOT) and serum alanine transaminase (SGPT) and histopathological microscopic examination. The hepatoprotective effects of various concentration of PEE on liver damage induced by hepatotoxic dose (300 mg/kg) of econazole were observed by the obvious decrement of SGOT and SGPT level and further confirmed by hepatohistological microscopic examination. The inhibitory effects of PEE on FeCl2-induced (in vitro) or econazole-induced (in vivo) lipid peroxidation were investigated from the measurement of the formed malonic dialdehyde (MDA) level in the rat liver homogenate. The IC50 (μM) of various concentrations of PEE in the superoxide scavenging activity in econazole (300 mg/kg)-damaged rat liver homogenate were assessed by cytochrome c reduction method and compared with that of (+)-alpha-tocopherol. It could be postulated that the hepatoprotective effect of PEE may be, at least in part, due to their inhibitory ability on membrane lipid peroxidation and free radical formation or due to their free radical scavenging ability.

The antioxidative effect of hot water extract of the mushroom Ganoderma lucidum on ethanol-induced free radical generation had been studied. In order to further investigate the hepatic and renal protective mechanism of Ganoderma lucidum, rates of lipid peroxidation were determined. The hot water extract of Ganoderma lucidum dose-dependently exhibited antioxidative effect on mouse liver and kidney lipid peroxidation; our results indicated that hepatic and renal homogenates have a higher malonic dialdehyde level in an ethanol administered group than in the Ganoderma lucidum treated group. It was concluded that the hepatic and renal protective mechanism of Ganoderma lucidum, might be due at least in part to its prominent superoxide scavenging effect. Ganoderma extract could protect the liver and kidney from superoxide induced hepatic and renal damages.

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.

Acute p.o. administration of 99.5% ethanol (0.1 ml) to fasted mice produced heart toxicity. Pretreatment with p.o. administration of tetramethylpyrazine (TMP) could prevent such toxicity effectively and dose-dependently. The maximal antioxidative effect against 99.5% ethanol-induced heart toxicity could be observed at 1 hour after TMP administration. In order to further investigate the heart protective mechanism of TMP, both lipid peroxidation level in vivo and superoxide scavenging activity were conducted. TMP exhibited a dose-dependently anti-lipid peroxidation effect in mice heart homogenate, and results indicated that 99.5% ethanol-induced intoxicated mice hearts have higher malonic dialdehyde (MDA) levels compared with those in TMP administrated mice hearts. These results suggest that the potentially heart protective mechanism of TMP could be contributed, at least in part, to its prominent anti-lipid peroxidation and anti-free radical formation effects, hence it could protect the heart from lipid peroxidation-induced heart toxicity.

Acute p.o. administration of absolute ethanol (10 ml/kg) to fasted mice would produce extensive renal failure. Pretreatment with p.o. administration of propolis ethanol extract (PEE) could prevent such renal failure effectively and dose dependently. This renal protective effect of PEE may be contributed, at least in part, to its antioxidative activity. The maximal antioxidative effect against absolute ethanol (AE)-induced renal failure could be observed 1 hour after PEE administration. In order to further investigate the renal protective mechanism of PEE, lipid peroxidation and superoxide scavenging activity were conducted in vivo. PEE exhibited dose-dependent antioxidative effects on lipid peroxidation in mice renal homogenate. Results indicated that mice with acute renal failure have higher malonic dialdehyde (MDA) levels compared with those in PEE administered mice. It was concluded that the renal protective mechanism of PEE could be contributed, at least in part, to its prominent superoxide scavenging effect; hence, it could protect, indirectly, the kidney from superoxide-induced renal damages.

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.