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Oxidative stress and pyroptosis have been established as key contributors to myocardial ischemia-reperfusion injury (MIRI). While previous studies reported that electroacupuncture (EA) preconditioning exerted cardioprotective effects, the underlying mechanisms remain elusive. Thus, this study aimed to investigate the effects of EA preconditioning on oxidative stress and pyroptosis in MIRI rats, and explore the role of nuclear factor E2-associated factor 2 (Nrf2) throughout that process. A MIRI model was constructed by ligating the left anterior descending coronary artery for 30 min, followed by 4 h of reperfusion in rats. Prior to modeling, rats were subjected to EA at the Neiguan Point for three days. Furthermore, ML385, a Nrf2 inhibitor, was administered in order to examine the role of Nrf2 in regulating oxidative stress and pyroptosis following EA preconditioning. The results revealed that EA preconditioning improved left ventricular function after MIRI and reduced both the myocardial infarction area and cTnT levels. Meanwhile, EA preconditioning alleviated MIRI-induced oxidative stress and pyroptosis, as evidenced by the downregulation of ROS, MDA, NF-$\kappa$B p65, caspase-1, IL-1$\beta$, and GSDMD-N, and the upregulation of SOD and HO-1. Mechanistically, EA up-regulated enhanced the expression of Nrf2. However, its cardioprotective effects and ability to attenuate oxidative stress and pyroptosis were suppressed by the inhibition of Nrf2. Taken together, our study indicated that EA preconditioning attenuated MIRI in rats by mitigating oxidative stress and pyroptosis, with Nrf2 playing a vital role in this protective mechanism.

Endometriosis (EMS) is a chronic, estrogen-dependent inflammatory disease affecting 5–10% of women of reproductive age, characterized by the growth of endometrial tissue on the outside of the uterus. The dysregulation of iron metabolism leads to the accumulation of iron ions at the lesion sites, resulting in oxidative stress and pro-inflammatory responses that promote the progression of EMS. The mechanisms underlying ferroptosis in EMS primarily involve iron accumulation, lipid peroxidation, and loss of glutathione peroxidase 4 activity. These mechanisms confer resistance to ferroptosis within the ectopic tissues and facilitate cell survival and proliferation. Traditional Chinese medicine (TCM) has demonstrated therapeutic potential for modulating ferroptosis. Studies have shown that TCM monomers may regulate ferroptosis by modulating iron transport proteins and anti-oxidant defense mechanisms. TCM formulas employ distinct treatment strategies depending on the stage of EMS: in the early stages, they promote ferroptosis to control lesion growth, whereas in the later stages, they inhibit ferroptosis to reduce oxidative stress and inflammation in order to improve reproductive health and slow disease progression. This study provides a new perspective on potential therapeutic strategies for the management of EMS by summarizing the role of ferroptosis in its pathological mechanisms and reviewing findings on the use of TCM in regulating ferroptosis.

Vanillic acid’s ability to effectively quench-free radicals has sparked widespread interest in its antioxidant potential. The title molecule’s structure was optimized using the Gaussian 16 program with the B3LYP/6-31+G($d$,$p)$ basis set. Natural bond orbital (NBO) calculations reveal that the O${}_{(2)}$-H${}_{(19)}$ bond in vanillic acid is labile, facilitating the generation of a free radical. The high-bond dissociation energy (BDE) of vanillic acid raises concerns about its efficacy as an antioxidant, particularly when compared to gallic acid (GA) and butylated hydroxy toluene (BHT). Introduction of electron-donating groups (EDGs) at the 10th position significantly enhanced the antioxidant activity of vanillic acid. Vanillic acid and its derivatives show enhanced safety profiles, outperforming BHT in toxicological studies. This paper presents a systematic investigation of vanillic acid and its derivatives, focusing on structural analysis, solvent effects, antioxidant mechanism and toxicological evaluation.

Cellular expression of the 70 kDa heat shock protein (HSP-70) is observed following hyperthermia and is correlated with transient resistance to subsequent heating. Photodynamic therapy (PDT) mediated oxidative stress can also induce transcriptional and translational expression of a variety of genes including HSP-70. However, PDT-mediated HSP-70 expression can vary as a function of photosensitizer type and incubation conditions. In the current study we used three clinically relevant photosensitizers, a porphyrin (Photofrin), a purpurin (SnET2), and a chlorin (NPe6), to examine PDT-mediated HSP-70 expression profiles and photosensitivity characteristics in parental radiation-induced fibrosarcoma cells (RIF-1) and in thermal resistant RIF-1 clones. We observed that in vitro PDT treatments using either SnET2 or NPe6 induced HSP-70 expression but that comparable PDT treatments using Photofrin did not result in increased HSP-70 levels. We also observed that PDT sensitivity in parental and heat-resistant cell clones were similar for each photosensitizer while thermal sensitivity was significantly reduced in the RIF clones which constitutively overexpressed HSP-70. These results indicate that definable differences can exist in the molecular pathways induced by PDT for different photosensitizers. Our results also demonstrate that constitutive overexpression of HSP-70 does not modulate PDT photosensitivity regardless of whether PDT treatments induce HSP-70 expression. We conclude that HSP-70 expression does not play a significant role in cellular PDT photosensitivity.

Oxidative injury caused by oxidatively modified low density lipoprotein (Ox-LDL) plays an important role in the transformation of macrophages into foam cells and atherogenesis. Treatments to protect macrophages from oxidative injury will be effective in treating atherosclerosis. A macrophage-specific growth factor, macrophage colony-stimulating factor (M-CSF), was reported to be able to prevent the progression of atherosclerosis in Watanabe heritable hypercholesterolemic (WHHL) rabbits. A protein-bound polysaccharide, polysaccharide Krestin (PSK), was also proven to have effects in preventing atherosclerosis in our previous work. We proposed that, both M-CSF and PSK could protect macrophages from oxidative injury, and the effects of PSK were associated with its capability of inducing M-CSF expression. In our present results, M-CSF could alleviate the Ox-LDL- or tert-butyl hydroperoxide (tbOOH)-induced injury to mouse peritoneal macrophages, and PSK exhibited some similar effects. PSK treatment could induce M-CSF gene expression and secretion in mouse peritoneal macrophages. Furthermore, actinomycin D and cycloheximide could attenuate that induction. We concluded that, maybe PSK exerted its effects on macrophages partly through the transcriptional induction of M-CSF in the cells.

The effects of Rosa rugosa on diabetic oxidative stress were investigated using rats with streptozotocin (STZ)-induced diabetes. The diabetic rats showed less body weight gain and heavier kidney and liver weights than normal rats, while the oral administration of Rosa rugosa at a dose of 100 or 200 mg/kg body weight/day for 20 days attenuated the physiological changes induced by diabetes. In addition, administrating Rosa rugosa to diabetic rats resulted in significant and dose-dependent decreases in the serum glucose and glycosylated protein levels, implying that Rosa rugosa improves the abnormal glucose metabolism that leads to oxidative stress. Diabetic rats had higher serum levels of superoxide and nitrite/nitrate. However, the administration of Rosa rugosa dose-dependently reduced the over-production of radicals associated with diabetes, suggesting Rosa rugosa is a radical scavenger that would play a crucial role in protecting against diabetic oxidative stress. Rosa rugosa significantly and dose-dependently reduced thiobarbituric acid-reactive substance levels in serum, hepatic and renal mitochondria, implying that Rosa rugosa would alleviate the oxidative stress associated with diabetes by inhibiting lipid peroxidation. This study provides evidence that Rosa rugosa has potential as a treatment for diabetes through attenuating oxidative stress induced by the diabetic condition

Oxidative stress can be implicated as a cause of liver fibrosis. In this sense, Ginkgo Biloba Extract (EGB), an antioxidant, may be beneficial in restraining liver fibrosis. The aim of this study was to evaluate the effects of EGB on experimental liver fibrosis. Rat liver fibrosis was induced by intraperitoneal injection of carbon tetrachloride (CCl₄) twice a week for 8 weeks. Three groups of rats received EGB (0.25, 0.5 and 1.0 g/kg, respectively) by stomach everyday. CCl₄ administration induced liver fibrosis, which was inhibited by EGB in a dose-dependent manner. The histopathologic score of fibrosis, liver function and the levels of plasma hyaluronic acid (HA) and laminin (LN) were significantly improved in rats treated with CCl₄ + EGB, compared with those treated with CCl₄ only (p < 0.01 or p < 0.05). The activities of superoxide dismutase (SOD) and glutathione pero xidase (GSH-Px) were notably elevated, while malondialdehyde (MDA) content was significantly decreased in the rats treated with CCl₄ + EGB (p < 0.01 or p < 0.05). Inhibition of hepatic stellate cell (HSC) activation and nuclear factor kappaBP₆₅ (NF-κBP₆₅) expression was demonstrated in the livers of EGB-treated rats. The activation of NF-κB was significantly suppressed in EGB-treated rats determined by electrophoretic mobility shift assay (EMSA). Furthermore, EGB reduced expressions of transforming growth factor-β₁ (TGF-β₁) and collagen I mRNA. In conclusion, EGB is able to ameliorate liver injury and prevent rats from CCl₄-induced liver fibrosis by suppressing oxidative stress. This process may be related to inhibiting the induction of NF-κB on HSC activation and the expression of TGF-β₁.

Oxidative stress plays a key role in the pathophysiologic process of acute and chronic renal diseases. Intracellular component such as lipids, proteins and nucleic acids are easily and rapidly oxidized by excessive reactive oxygen species (ROS), and such reactions lead to increased levels of lipid peroxide. The present study examined the antioxidant effects of Wen-Pi-Tang and its component crude drugs on 2,2′-azobis(2-amidinopropane) dihydrochloride (AAPH)- or 2,2′-azobis(2,4-dimethylvaleronitrile) (AMVN)-induced ROS generation and lipid peroxidation of linoleic acid. As a result, Wen-Pi-Tang significantly decreased AAPH or AMVN-induced ROS in renal mitochondrial particles. For the components in Wen-Pi-Tang's prescription, Rhei Rhizoma and Glycyrrhizae Radix extracts strongly inhibited peroxide levels, but Ginseng Radix, Aconiti Tuber and Zingiberis Rhizoma extracts were comparably low. Rhei Rhizoma extract showed the strongest inhibitory activity on oxidative injury, and two of its tannin compounds, (-)-epicatechin 3-O-gallate and procyanidin B-2 3,3′-di-O-gallate, inhibited AAPH or AMVN-induced ROS significantly. Thus, the present data suggest that Wen-Pi-Tang and its component crude drugs effectively prevent biological toxicity on oxidative stress through potent antioxidant and anti-lipid peroxidation activities.

Picroside II is an active constituent extracted from the traditional Chinese medicine (TCM) Hu-Huang-Lian. To evaluate the neuroprotective effect of picroside II, PC12 cells were treated with glutamate in vitro and male ICR mice were treated with AlCl₃in vivo. Pre-treatment of PC12 cells with picroside II could enhance the cell viability and decrease the level of intracellular reactive oxygen species (ROS) induced by glutamate. By DNA fragmentation and flow cytometry assay, picroside II (1.2 mg/ml) significantly prevented glutamate-induced cell apoptosis. In the animal study, amnesia was induced in mice by AlCl₃ (100 mg/kg/d, i.v.). Pricroside II, at the dose of 20 and 40 mg/kg/d (i.g.), markedly ameliorated AlCl₃-induced learning and memory dysfunctions and attenuated AlCl₃-induced histological changes. This was associated with the significant increased superoxide dismutase (SOD) activity in the brain of experimental mice. All these results indicated that picroside II possessed the therapeutic potential in protecting against neurological injuries damaged by oxidative stress.

Apoptosis was demonstrated to be a major mode of intestinal epithelial cell death caused by intestinal ischemia/reperfusion (II/R). Ceramide has been proposed as a messenger for apoptosis. The present study was aimed to investigate the effect of Ginkgo biloba extract 761 (EGb 761) pretreatment on II/R-induced intestinal mucosal epithelial apoptosis in rats and the mechanism related to ceramide. The rat model of II/R injury was produced by clamping superior mesenteric artery for 60 min followed by reperfusion for 180 min. Twenty four rats were randomly allocated into Sham, II/R and EGb + II/R groups. In EGb + II/R group, EGb 761 (100 mg/kg per day) was administered intragastrically for 7 days before the surgery. Animals in II/R and sham groups were treated with equal volume of normal saline solution. Intestinal mucosal epithelial apoptosis was detected via electron microscopy and TUNEL method. Lipid peroxidation in intestinal mucosa was determined by detecting the malondialdehyde level and the activities of superoxide dismutase and peroxidase glutathione. The ceramide generation and sphingomyelinase (SMase) mRNA expression in intestinal mucosa were determined by high performance, thin layer chromatography, and RT-PCR, respectively. II/R caused intestinal mucosal epithelial apoptosis and over-production of the ceramide accompanied by up-regulation of SMase mRNA expression and increases of lipid peroxidation. EGb 761 pretreatment significantly decreased apoptosis index, and concurrently reduced the ceramide generation accompanied by down-regulation of SMase expression and inhibition of lipid peroxidation. The findings indicate that EGb 761 pretreatment attenuates II/R-induced intestinal epithelial apoptosis, which might be attributable to its antioxidant action of mediating ceramide pathway.

Chloramphenicol is a toxic antibiotic used for certain infections, though aplastic anaemia is one of its side-effects. The results of our experiments showed that blood cells suffered oxidative stress in the presence of chloramphenicol, with a significant increase in reactive oxygen species (ROS) detected by luminol-chemiluminescence (CL). The extract of fruits of Eriobotrya japonica markedly decreased ROS in leukocytes and erythrocytes, the oxidative stress caused by this antibiotic. Nitro Blue Tetrazolium (NBT) assay with purified leukocytes demonstrated that the antioxidant action of E. japonica caused an intracellular reduction in ROS, and that the extracts decreased these promoters of oxidative stress to normal levels in the cytoplasm. Determinations of nitric oxide (NO) generation indicated that E. japonica extracts also inhibited the stimuli of NO provoked by chloramphenicol. This study showed that the immediate antioxidant effect of E. japonica could be associated with the action of vitamin A. The protective action of this fruit was seen on mature leukocytes and erythrocytes, beneficial effect on blood cells suggest that its extract could be used as an antioxidant agent complementing the administration of chloramphenicol, as a modern-day extension to its traditional use in Chinese medicine.

Euonymus alatus (E. alatus) has been used as a folk medicine for diabetes in China for more than one thousand years. In order to identify major active components, effects of different fractions of E. alatus on the plasma glucose levels were investigated in normal mice and alloxan-induced diabetic mice. Our results show that ethyl acetate fraction (EtOAc Fr.) displayed significant effects on reducing plasma glucose. In oral glucose tolerance, EtOAc Fr. at 17.2 mg/kg could significantly decrease the blood glucose of both normal mice and diabetic mice. After 4 weeks administration of the EtOAc Fr, when compared with the diabetic control, there were significant difference in biochemical parameters, such as glycosylated serum protein, superoxide dismutase and malondial dehyde, triglyceride, and total cholesterol, between alloxan-induced diabetic mice and the control group. Additional histopathological studies of pancreatic islets also showed EtOAc Fr. has beneficial effects on diabetic mice. Chemical analysis with three-dimensional HPLC demonstrated that the major components from EtOAc Fr were flavonoids and phenolic acids, which had anti-oxidative effects on scavenging DPPH-radical in vitro. All these experimental results suggest that EtOAc Fr. is an active fraction of E. alatus and can prevent the progress of diabetes. The mechanism of E. alatus for glucose control may be by stimulating insulin release, improving glucose uptake and improving oxidative-stress.

This study was to investigate the protective effects and possible mechanisms of total flavones of rhododendra (TFR) against cerebral ischemia reperfusion injury in rats and mice. Cerebral ischemia/reperfusion injury was induced by occluding the right middle cerebral artery (MCA). Infarct volume, neurological deficit, brain water content, levels of malondialdehyde (MDA), nitric oxide (NO) contents, lactate dehydrogenase (LDH) activity in plasma and brain, levels of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities and mRNA expression of inducible nitric oxide synthase (iNOS), neuronal nitric oxide synthase (nNOS) and endothelial nitric oxide synthase (eNOS) in brain were evaluated 7 or 10 days after treatment. TFR significantly reduced infarct volume, ameliorated the neurological deficit and reduced the brain water content. The activities of SOD, LDH and GPX in brain were enhanced, while the activity of LDH in plasma and the contents of MDA and NO in plasma and brain were decreased. While, the expression of iNOS and nNOS mRNA in brain were down-regulated, the expression of eNOS mRNA in the brain was up-regulated. These results suggest that TFR has protective effects for cerebral injury in rats and mice, which might be associated with its antioxidant properties and ability to regulate the expression of NOS isoforms.

Oxidative stress is the root cause of diabetic macro- and microvascular complications. Biochemical and epidemiological studies indicate that current treatments for diabetes do not reduce risks of developing complications, suggesting their inability to alleviate the levels of oxidative stress. This study in streptozotocin (STZ)-induced diabetic rats was carried out to investigate the effect of combining the antidiabetic drug, metformin, with an ethanolic extract of Scutellaria baicalensis, a plant whose root is known for its radical scavenging activity. Three groups of STZ-induced diabetic rats were given the following treatments for 30 days: (1) metformin 500 mg/kg, (2) S. baicalensis 400 mg/kg, (3) metformin 500 mg/kg + S. baicalensis extract 400 mg/kg. In addition, vehicle-treated diabetic and nondiabetic controls were used in the experiment. The rats treated with S. baicalensis and metformin + S. baicalensis had elevated hepatic activities of the antioxidant enzymes — superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) compared to the vehicle- and metformin-treated diabetic groups (p < 0.05). Plasma and hepatic lipid peroxide concentrations in the herb-treated and herb + metformin-treated groups were also significantly reduced (p < 0.05). In addition, the combined treatment caused significant elevations of plasma and pancreatic insulin levels and reductions of plasma and hepatic triglycerides (TG) and cholesterol levels. The study thus showed that S. baicalensis enhanced the antidiabetic effect of metformin in STZ-induced diabetic rats by improving the antioxidant status. It also increased pancreatic insulin content as well as improved the lipid profile in these rats.

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.

To investigate the effects of Korean ginseng (KG, Panax ginseng C.A. Meyer) and heat-processed Korean ginseng (H-KG) on diabetic renal damage, we used the streptozotocin-induced diabetic rat model in this study. The diabetes-induced physiological abnormalities at early-stage were attenuated by KG or H-KG administration through reducing the blood glucose level and improving renal function. The oxidative stress-induced increases in serum and renal thiobarbituric acid-reactive substance levels were significantly reduced by KG and H-KG administrations. Moreover, the protein expressions related to oxidative stress and advanced glycation endproducts were significantly reduced in diabetic rats and/or not significantly increased compared to normal rats by KG or H-KG administration. All of these beneficial effects of H-KG in diabetic rats were stronger than those of KG. Therefore, KG and H-KG may improve diabetic pathological conditions and prevent renal damage associated with diabetic nephropathy, and these protective effects of KG can be improved by heat-processing. This study provides scientific evidence that H-KG may be a potential therapeutic agent for pathological conditions associated with diabetic complications including diabetic nephropathy.

To evaluate the effect of gingko biloba (EGb) on diethylstilbestrol (DES) induced testicle injury in mice. Fifty male mice were divided into a control group (A), DES group (B), and 3 EGb groups (C, D, E). The EGb-treated groups received peritoneal EGb at 8.75 (C), 17.5 (D), 35 mg/kg (E) BW daily for 7 days. The control group was given equivalent amount of normal saline. The mice in groups B, C, D and E were injected hypodermically with DES at 40 mg/kg BW daily 4 hours after the first herbal administration, while the control was given olive oil. Compared with DES group, the testis coefficients-relative testicular weight increased in the three EGb-treated groups. No significant difference was observed in epididymis coefficients. Lipid peroxidation status and antioxidant enzyme activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were significantly elevated in testes of EGb-treated groups. Lactate dehydrogenase (LDH) activities and malonaldehyde (MDA) contents were significantly decreased in testes of the EGb groups. The results indicate that EGb protects the testis from diethylstilbestrol-induced injury.

Adaptogens are harmless herbs which have pharmaceutical benefits due to their balancing, regulative and tonic functions. However, despite these medicinal effects, the antioxidant potential of adaptogens is rarely mentioned. This study investigated the antioxidant potential of 3 adaptogen extracts, Rhodiola rosea (golden root), Eleutherococcus senticosis (Siberian ginseng) and Emblica officinalis (Indian gooseberry, Amla). The results of this study showed that R. rosea had the highest potential for singlet oxygen scavenging, hydrogen peroxide scavenging, ferric reducing, ferrous chelating and protein thiol protection than either of the other 2 extracts. E. senticosis, on the other hand, showed the best potential for hypochlorite scavenging. In addition, the polyphenol content in the 3 adaptogen extracts followed the order: R. rosea, E. officinalis and E. senticosis. Our data suggest that the antioxidant potential of the 3 adaptogen extracts was proportional to their respective polyphenol content. The supplementation of adaptogen extracts containing high levels of polyphenols may not only have adaptogen properties, but may decrease the risk of complications induced by oxidative stress.

Emblica Officinalis (also known as Amla or Indian Gooseberry), a natural, traditional and functional food in Asia, has physiological benefits such as hepato-, cyto- and radio- protection, as well as hypolipidemic effects. In addition, Amla often functions as a potent antioxidant due to the high level of ascorbic acid (ranging from 1,100 to 1,700 mg/100 g of fruit) in its fruit. The aim of this study was to determine whether supplementation with Amla extract could reduce oxidative stress in patients with uremia. The findings show that supplementation with Amla extract for 4 months reduced the plasma oxidative marker, 8-iso-prostaglandin, (M0 vs. M4 = 1415 ± 1234 pg/ml vs. 750 ± 496 pg/ml, p < 0.05) and increased plasma total antioxidant status (TAS) (M0 vs. M4 = 2.32 ± 0.14 mM vs. 2.55 ± 0.24 mM, p < 0.05) in uremic patients. On the other hand, there were no significant differences observed in liver function (GOP and GPT), renal function (creatinine, blood urea nitrogen and uric acid), diabetic index (plasma glucose and adiponectin) and atherogenic index (LDL/HDL ratio, total cholesterol and homocysteine) in patients treated with Amla for 4 months. Our data suggest that Amla supplementation may increase plasma antioxidant power and decrease oxidative stress in uremic patients. However, Amla extract did not influence hepatic or renal function, or diabetic and atherogenic indices in uremic patients.

Reactive oxygen species (ROS) and their derivatives play important roles in the development of diseases such as, cardiovascular disease, ischemic disease, and aging. Much effort has been devoted to finding both an effective and non-toxic antioxidant traditional Chinese medicine (TCM) herbal formula. Tianwang Buxin Pills (TBPs) have been used in TCM to treat mild cognitive impairment and palpitations. Recently, research has revealed that TBPs are effective against oxidative stress and psychological stress in experimental studies. However, randomized controlled trials (RCT) are rare. This study was conducted to assess the antioxidative and anti-stress effects of TBPs by analyzing (determination) reactive oxygen metabolites (d-ROMs test) of the blood, the stress response inventory (SRI), and the Korean version of the WHO Quality of Life Scale Abbreviated Version (WHOQOL-BREF) in 39 healthy volunteers (Placebo group = 20, TBPs group = 19) before and after oral administration of TBPs for 4 weeks. However, d-ROMs test, SRI, and WHOQOL-BREF values did not differ significantly between the two groups. These results indicate that TBPs do not effectively restrain ROS or their derivatives.