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Little is known about the effect of far-infrared rays (FIR) on serotonin and malondialdehyde levels in depressed patients with insomnia. The purpose of this study is to assess the effect of far-infrared rays on depressed people with insomnia. A randomized design was used to determine this effect. A total of 70 inpatients were recruited with the clinical diagnosis of depression with sleep disturbance. In the experimental group, FIR was applied to three chosen acupuncture points by a patch-like sticker for a period of 15 minutes twice a week. The three acupuncture points are Nei-Kuan (PC6), Shenmen (HT7) and Sanyinjiao (SP6). The total duration of experiment was four weeks. For both experimental and control groups, serum levels of serotonin (5HT) and malondialdehyde (MDA) were examined before and after the introduction of FIR. The experimental group revealed disparate changes over different dependent variables, in which serotonin increased but MDA decreased after the introduction of FIR. These observations indicate that the serotonin pathway is involved in the pathophysiological mechanism responsible for the damaging effects of MDA on depressed patients with insomnia.

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 purpose of this study was to examine whether the symptoms of dysmenorrhea in young women were related to serum malondialdehyde (MDA) and interleukin-6 (IL-6) levels. Ninety-four non-smoking and non-drinking female subjects without serious disease from a nursing college in Taiwan were divided into two groups. Group 1 consisted of 51 subjects without dysmenorrheal, and Group 2 of 43 subjects with dysmenorrheal symptom. All subjects were provided informed consent. Results showed that the serum levels of MDA and of IL-6 were significantly different between the two groups (P < 0.05) and (P < 0.005), respectively. We conclude that the pathological mechanism of dysmenorrhea is mediated by oxidative stress caused by the action of cytokine.

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.

Acute oral administration of absolute ethanol (1.0 ml/kg) to fasting rats produced extensive necrosis of the gastric mucosa within 1 h. Pretreatment 30 min before administration of ethanol with oral tetramethylpyrazine (TMP) prevented this necrosis. Gross examination of the gastric mucosa of rats that received TMP showed fewer gastric lesions than that of rats who did not receive TMP. TMP pretreatment in rats exhibited superoxide scavenging activity in absolute ethanol-induced lipid peroxidation in gastric mucosal homogenates. TMP added in vitro to gastric homogenates made from control rats also showed scavenging activity. We conclude that the gastric protective mechanism of TMP could be attributed, at least in part, to its ability to inhibit lipid peroxidation and hence indirectly protect the gastric mucosa from oxidative stress.

Oxygen free radicals have been suggested to be a contributory factor in complications of diabetes mellitus. In the present study, we investigated the effect of tetramethylpyrazine (TMP) (10, 25 and 50 mg/kg), an active component of a Chinese medicinal plant Ligusticum wallich Franch (Chuanxiang), on streptozotocin (STZ)-induced diabetic male ICR mice. STZ was injected as a single daily dose (4 mg/kg i.p. in buffered citrate solution, pH 4.0) for one week. A single daily dose of TMP (10, 25 or 50 mg/kg i.p.) was administered for 2 weeks to the STZ-induced diabetic mice immediately following 1 week STZ induction. Plasma glucose and serum blood urea nitrogen (BUN) concentrations were estimated at the time of sacrifice. Malonialdehyde (MDA) formation was measured from the liver and kidney tissues. TMP dose dependently inhibited glucose concentration and BUN elevation. TMP also remarkably reduced the degree of lipoperoxidation. Our results indicate that TMP may be an effective agent for treatment of diabetes mellitus complications with oxidative stress.

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.

In this study, the intraperitoneal administration of 1 mg/kg thioacetamide (TAA) produced hepatotoxicity in mice. The increase in serum SGOT and SGPT produced at 24 h by this regimen was decreased in a dose-dependent manner by coadministration of tetramethylpyrazine (TMP; 10, 25 and 50 mg/kg). A rise in serum interleukin-2 was similarly prevented. Increased concentrations of malondialdehyde (MDA) generated in vitro in liver homogenates prepared from TAA-treated mice were decreased by TMP treatments. The increase in MDA produced by TAA was also prevented by in vitro addition of TMP to liver homogenates. These results suggest that part of the hepatocellular injury induced by TAA is mediated by oxidative stress caused by the action of cytokines through lipid peroxidation. TMP appears to act by preventing lipid peroxidation.

Acute administration of absolute ethanol (10 ml/kg) per os to fasted mice produced extensive renal failure as measured by a rise in blood urea nitrogen and creatinine. Pretreatment with oral administration of tetramethylpyrazine (TMP) prevented such failure. The maximal effect against absolute ethanol-induced renal failure could be observed 1 h after TMP administration. In order to further investigate the renal protective mechanism of TMP, experiments on lipid peroxidation and superoxide scavenging activity were conducted. Renal homogenates made from mice treated with ethanol showed that TMP pretreatment had an antioxidant effect. Mice in acute renal failure had higher malonic dialdehyde concentrations than those pretreated with TMP. The renal protective mechanism of TMP was attributed, in part, to its prominent superoxide scavenging effect, which protects the kidney from superoxide-induced renal damage.

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.

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.