The American Journal of Chinese Medicine

The objective of this study was to compare the acupoint infrared radiation spectrums of patients and healthy volunteers to show whether those of coronary heart disease (CHD) patients carry distinctive pathological information. PHE201, using a highly sensitive infrared spectrum detection device applied to the acupoint Neiguan (PC6) and to a control point on 50 CHD patients and 47 healthy adults. A total of 73 wavelength spots were detected. The scanned wavelengths ranged from 1.5 μm to 16 μm, and the scanning spacing was 0.2 μm. The data were automatically recorded in the database of the device for statistical analysis. Infrared radiation intensities of 23 in the 73 detected wavelength spots significantly differed in the CHD patients' Neiguan as compared to those of the healthy subjects (from p = 0.048 to p = 0.002), while only 12 wavelength spots at a non-acupuncture control point showed significant differences. By the χ² test, these differences between Neiguan and the non-acupuncture control point are statistically significant (p = 0.033). At 2-2.5 μm, which is related to energy metabolism, the intensity at the CHD patients' Neiguan was significantly lower than that of the healthy adults (from p = 0.026 to p = 0.017). No difference was observed at the non-acupuncture control point (from p = 0.094 to p = 0.052). The data suggest that the changes of infrared spectrum at Neiguan in coronary heart disease patients may reflect the distinct pathological changes. This may be the result of hypoactive energy metabolism in the area of the acupoint.

Our previous study has demonstrated that 6 weeks of Tai Chi exercise significantly improves knee pain and stiffness in elderly with knee osteoarthritis. This study also examine the effects of Tai Chi exercise on gait kinematics, physical function, pain, and pain self-efficacy in elderly with knee osteoarthritis. In this prospective, pretest-posttest clinical trial, 40 men and women (64.4 ± 8.3 years) diagnosed with knee osteoarthritis participated in 6 weeks of instructed Tai Chi training, 1 hour/session, 2 sessions/week. The following measures were taken at baseline and the conclusion of the intervention: (a) gait kinematics including stride length, stride frequency, and gait speed quantified using video analysis, (b) physical function, (c) knee pain, and (d) pain self-efficacy. Data were analyzed using repeated MANCOVA, MANOVA, ANOVA and Wilcoxon tests. After 6 weeks of Tai Chi exercise, stride length (p = 0.023; 1.17 ± 0.17 vs. 1.20 ± 0.14 m), stride frequency (p = 0.014; 0.91 ± 0.08 vs. 0.93 ± 0.08 strides/s), and consequently gait speed (p < 0.025; 1.06 ± 0.19 vs. 1.12 ± 0.15 m/s) increased in the participants. Physical function was significantly improved (p < 0.001) and knee pain was significantly decreased (p = 0.002), while no change was observed in pain self-efficacy. In conclusion, these findings support that Tai Chi is beneficial for gait kinematics in elderly with knee osteoarthritis, and a longer term application is needed to substantiate the effect of Tai Chi as an alternative exercise in management of knee osteoarthritis.

The purpose of this systemic review is to assess the efficacy of Er-xian decoction (EXD), a formula of Chinese medicine, in relieving menopausal symptoms. Seven databases were extensively retrieved. The Chinese electronic databases include VIP Information, CBMdisc, and CNKI. The English electronic databases include AMED, CINAHL, Cochrane Library, and MEDLINE. Randomized controlled trials using EXD as a main intervention were included in the study selection. The quality of studies was assessed by Jadad scale and the criteria referred in Cochrane reviewers' handbook. Two independent reviewers were responsible for data extraction and assessment. Discrepancies were rectified referring to the original articles. The efficacy of EXD treatment for menopausal symptoms was evaluated by meta-analysis. There were 154 articles retrieved according to the search strategy, 677 participants involved in the 5 studies that satisfied the selection criteria. Meta-analysis indicated that administration of EXD significantly relieved at least one menopausal symptom when compared to the control group at a 95% confidence interval (p < 0.01). The curing effect of EXD with all symptoms relieved was significant as compared with the control groups (p < 0.01). The results also indicated that the efficacy of EXD was better than the other non-menopausal hormone therapy (p < 0.01), while there was no significant difference between the EXD and menopausal hormone therapy groups. The EXD is effective in treating menopausal symptoms. However, owing to the low quality of the investigated studies, more randomized controlled trials are needed before evidence-based recommendation regarding the effectiveness of EXD in the management of menopausal symptoms can be provided.

Tyrosinase and its transcriptional regulator microphthalmia-associated transcription factor (MITF) play critical roles in regulation of melanogenesis, and are required for environmental cues or agents in modulation of melanin synthesis. Identifying the signals regulating tyrosinase and MITF is crucial to understanding how pigmentation responds to extracellular stimuli. In this report, we discovered that paeonol down-regulated melanin production via decreasing MITF expression and consequent mRNA and protein levels of tyrosinase. We also found that paeonol reduced phosphorylation of a cAMP responsive element binding protein (phospho-CREB), which binds and activates MITF. A selective inhibitor of c-jun N-terminal or stress-activated protein kinases (JNK/SAPK)-SP600125 significantly reversed paeonol-induced down-regulation of melanogenesis. Inhibition of cAMP/PKA pathway intensified the hypopigmentation response to paeonol. These results identify a mechanism in which paeonol induces the down-regulation of melanogenesis through inhibition of CREB phosphorylation, leading to the expression reduction of MITF and subsequently tyrosinase. The key kinase mediating the effects of paeonol on melanogenesis in B16F10 cells is JNK/SAPK. Additionally, the cAMP/PKA pathway may take part in this process.

Grifola frondosa, an edible fungus with a large fruiting body and overlapping caps, has been demonstrated to be a natural source of health-promoting substances, mainly due to its polysaccharides β-glucan. By using male Wistar rats injected with saline (normal rats) or nicotinamide plus streptozotocin (diabetic rats), we investigated the effects of an orally ingested placebo (CON and STZ groups), culture mycelium (CGM and SGM groups), broth (CGB and SGB groups), and mycelium plus broth (CGX and SGX groups) of Grifola frondosa on glycemic responses. During the experimental period (from day 0 to day 15), the STZ group had significantly lower body weight compared to the CON group (one-way ANOVA, p < 0.05). Moreover, the STZ group had significantly higher blood glucose concentrations at 2 hour-postprandial periods on days 0, 7, and 14 and in an oral glucose tolerance test (OGTT) on day 10, as well as significantly higher serum fructosamine and triglyceride on day 15 compared to the CON group. These diabetes-induced increases were significantly attenuated by administrations of mycelium and/or broth, i.e., the SGM, SGB, and SGX groups. The results of repeated-measures analysis and three-way ANOVA indicated that diabetes mellitus significantly increases, and mycelium administration significantly decreases postprandial blood glucose; diabetes mellitus significantly increases, and mycelium and broth administrations significantly decrease serum triglyceride, fructosamine, and blood glucose concentrations; moreover, in the area under the curve in OGTT, p < 0.05. Our results revealed that submerged-culture mycelia and broth of Grifola frondosa have bioactivities for improving glycemic responses.

To investigate whether HT008-1, a prescription used in traditional Korean medicine to treat mental and physical weakness, has a neuroprotective effect on a rat model of global brain ischemia and an enhancing effect against memory deficit following ischemia. Global brain ischemia was induced for 10 min by using 4-vessel occlusion (4-VO). HT008-1 was orally administered at doses of 30, 100, and 300 mg/kg respectively twice at 0 and 90 min after ischemia. The effect on memory deficit was investigated by using a Y-maze neurobehavioral test 4 days after brain ischemia, and the effect on neuronal damage was measured 7 days after ischemia. The mechanism of action was studied immunohistochemically using an anti-CD11b (OX-42) antibody. The oral administration of HT008-1 at 100 and 300 mg/kg significantly reduced hippocampal neuronal cell death by 49% and 53%, respectively, compared with a vehicle-treated group, and also improved spatial memory function in the Y-maze test. Immunohistochemically, HT008-1 inhibited OX-42 expression in the hippocampus. The effects of HT008-1 were more pronounced than those of its individual herb components. The herbal mixture HT008-1 protects the most vulnerable CA1 pyramidal cells of the hippocampus and enhances spatial memory function against global brain ischemia; an anti-inflammatory effect may be one of the mechanisms of action.

Baicalin is a flavonoid present in many traditional Chinese medicines. A number of studies show that baicalin has anti-inflammatory actions and protects against a variety of tissue and organ injuries. The effect of baicalin in lipopolysaccharide (LPS)-induced acute lung injury is not well studied. In this study, typically acute lung injury was induced in rat by intratracheal injection of LPS, which increased lactate dehydrogenase activity and protein content in bronchoalveolar lavage fluid, wet/dry lung weight ratio, Evan's blue dye leakage, and neutrophil infiltration. Baicalin (20 mg/kg) was administrated 1 hour before or 30 min after LPS injection. Both pre and post-treatment with baicalin attenuated the increase of these parameters and improved histological finding. Our results suggest that baicalin has a therapeutic effect on LPS-induced acute lung injury.

Salvia miltiorrhiza and Panax notoginseng were both considered to be beneficial to cardiovascular diseases in traditional Chinese medicine and often used in combination. To examine the possible interaction between them, the effects of the active fractions of these two herbs, salvianolic acids (SA) and notoginsengnosides (NG), on platelet aggregation were checked respectively or in combination in vitro and in vivo. Both the platelet aggregation of platelet rich plasma (PRP) and washed platelet after ADP induction were checked. In vitro study showed that both SA and NG had an inhibitory effect on platelet aggregation. However, there is no synergistic effect of the combination of SA and NG in vitro. In vivo study showed that i.g. 550 mg/kg/day SA or NG for 5 days could significantly inhibit ADP-induced platelet aggregation of PRP. Moreover, combination of SA and NG at a ratio of 5:1 had a synergistic effect on platelet aggregation of PRP. The mechanism for the synergism of SA and NG in vivo was not clear. High performance liquid chromatography analysis of the plasma of rats received SA, NG or combination of SA and NG showed that co-administration of NG caused change in the plasma distribution profile of SA. The influence of combination on the absorption and/or metabolism of SA may be one of the reasons for the synergism of SA and NG in vivo.

The clinical and pharmacological activities of ginseng are known to modulate immune function, metabolic processes and neuro-endocrine system activities. Ginseng saponins are the principle active ingredients in the formation of immune stimulating complexes. The objective of this study was to evaluate the in vitro effect of ginseng total saponin (GTS) on the phagocytic capacity of canine peripheral blood phagocytes. GTS itself did not cause any direct effect on the phagocytic capacity of peripheral blood mononuclear cells (PBMC) and polymorphonuclear cells (PMN) but not peripheral blood monocytes. However, the phagocytic capacity of PMN and monocytes, but not PBMC, was enhanced by the culture supernatant from PBMC treated with GTS. The phagocytic capacity of PMN and monocytes was also increased by treatment with recombinant canine (rc) tumor necrosis factor (TNF)-α. The ability of the culture supernatant from GTS-treated PBMC to stimulate the phagocytic capacity of phagocytes was inhibited by addition of anti-rc TNF-α polyclonal antibody (pAb) prior to the culture. The amount of TNF-α in the culture supernatant from PBMC was shown to increase upon treatment of GTS as compared with that of vehicle-treated PBMC culture supernatant. These results suggest that GTS has an immunoenhancing effect on the phagocytic capacity of canine peripheral blood phagocytes, which is mainly mediated by TNF-α released from GTS-stimulated PBMC.

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.

Cirsium arisanense Kitamura (Compositae) has been used for hundreds of years in Taiwan as a folk medicine for hepatoprotection. However, no scientific research has demonstrated this effect. In the present study, we extracted the phenol-containing aqueous components of C. arisanense roots (CaR) and leaves/stem (CaL), and then assessed their hepatoprotective activities in both human hepatocellular carcinoma Hep 3B cells and C57BL/6 mice strain. High performance liquid chromatography (HPLC) analysis revealed that the components of CaR and CaL differed from those of the positive control silymarin. CaR exhibited a higher phenolic content and antioxidant capacity than CaL. Hep 3B cells treated with silymarin (0–200 μg/ml) demonstrated a concentration-dependent decrease in viability; however, both CaR and CaL did not exhibit any apparent cytotoxicity. Silymarin at 100 μg/ml, as well as CaR and CaL, not only protect Hep 3B cells from tacrine-induced hepatotoxicity but also decrease the expression of hepatitis B surface antigen (HBsAg). Moreover, an animal experiment demonstrated that CaR, CaL, and silymarin have hepatoprotective effects in C57BL/6 mice injected with tacrine, and they significantly decrease the levels of plasma alanine aminotransferase (ALT) and aspartate aminotransferase (AST). These effects of CaR and silymarin, but not of CaL, may occur via an increase in the hepatic glutathione level and the elimination of the nitric oxide production. In conclusion, the phenol-containing aqueous components from C. arisanense have potential in hepatoprotection.

This study was aimed to evaluate the antioxidant abilities of water (SGWE), 50% ethanolic (SGE50) and 95% ethanolic (SGE95) extracts from the stem of Graptopetalum paraguayense, and the extract with the highest antioxidant activity was assayed for its inhibitory effect on proliferation of human hepatoma (Hep G2) cell line. Antioxidant abilities of extracts were assessed their radical-scavenging abilities and effects on Fe/ascorbate-induced lipid peroxidation in a liposome model system. The results of this study showed that antioxidant activities were increased with the increase of the extracts concentrations, and the activities correlated with both the total phenol and anthocyanin contents. A comparison of the 50% inhibition concentration (IC₅₀) values of different antioxidant reactions revealed that SGWE was the more effective at scavenging superoxide anion radical and preventing lipid peroxidation than SGE50 and SGE95 (p < 0.05). The flow cytometry results indicated that SGWE lowered cell viability, and induced G1 phase arrest and apoptosis in Hep G2 cells. These results demonstrated the antioxidatant and anti-hepatoma potential of stem of Graptopetalum paraguayense.

This study was aimed at investigating the protective effect and mechanism of vitexin preconditioning (VPC) on cultured neonatal rat cardiomyocytes after anoxia and reoxygenation (A/R). An A/R model was established by using cultured neonatal rat cardiomyocytes. Cellular injury was evaluated by measuring cell viability, the releases of creatine kinase (CK), and lactate dehydrogenase (LDH). The apoptosis rate of cardiomyocytes after Anoxia/reoxygenation and the activities of extracellular signal-regulated protein kinases (ERKs) were measured. The intracellular calcium indicated by the fluorescence in cardiomyocytes was measured by the laser confocal microscope. Vitexin preconditioning (10, 30 and 100 μM) significantly enhanced the cell viability, markedly inhibited A/R-induced increases of LDH and CK release, obviously decreased the number of apoptotic cardiomyocytes and markedly decreased the fluorescence intensity value of [Ca²⁺]_i in cardiomyocytes. Exposure to anoxia or vitexin preconditioning significantly increased the phospho-ERK level, and the increase was markedly inhibited by PD98059, an inhibitor of the upstream kinase of ERK. These results suggest that vitexin preconditioning has a protective effect on cardiomyocytes A/R injury through the improvement of cell viability, decrease of LDH and CK release, such that the protective mechanism may relate to its ability to inhibit the cardiomyocytes apoptosis, reduce the cardiomyocytes calcium overload and increase the abundance of phosphor-ERK1/2 of the cardiomyocytes after anoxia and reoxygenation.

Since TNF-related apoptosis inducing ligand (TRAIL) is one of several apoptotic stimuli on articular chondrocytes, the modulation of the mechanism mediated by TRAIL could be considered as a novel strategy for the treatment of osteoarthritis (OA). Previous studies demonstrated that Clematis mandshurica prevents staurosporin-induced apoptosis in articular chondrocytes. This study was undertaken to examine whether Clematis mandshurica could prevent TRAIL-induced apoptosis in articular chondrocytes. Our data show that Clematis mandshurica prevents adenoviral TRAIL (Ad-TRAIL)-induced apoptosis in primary cultured articular chondrocytes. Clematis mandshurica prevents Ad-TRAIL-induced down-regulation of 14-3-3 and phosphorylated Akt. In addition, Clematis mandshurica treatment prevents the Ad-TRAIL-induced reduction of the interactions between 14-3-3 with phospho-ser112-Bad and phospho-ser136-Bad, and BcL-xL with phospho-ser155-Bad. A better understanding of the mechanism underlying inhibition of apoptosis in OA chondrocytes by Clematis mandshurica might lead to the development of a new therapeutic strategy for OA.

Blumea balsamifera (also known as sambong), a medicinal plant, is known to improve physiological disorders such as rheumatism and hypertension. However, its anticancer activity has not been well elucidated. In this study, we found that Blumea balsamiferaMeOH extract (BME) induced growth inhibitory activity in rat and human hepatocellular carcinoma cells (McA-RH7777, HepG2, respectively) without cytotoxicity as in with rat hepatocytes used as a normal cell model. BME induced cell cycle arrest at G1 phase via decreases in expression of cyclin-E and phosphorylation of retinoblastoma (Rb) protein in both dose- and time-dependent manners. Furthermore, BME reduced the level of a proliferation related ligand (APRIL) which stimulates tumor cell growth. The anti-proliferative effect of BME was improved slightly but significantly by the treatment with recombinant human APRIL. These findings suggest that BME may have a possible therapeutic potential in hepatoma cancer patients and the depletion of cellular APRIL may be one of the important mechanisms on the growth inhibitory effect of BME.

Aristolochic acid-II (AA-II) conjugated with bovine serum albumin (BSA) was used as an antigen for immunizing BALB/c mice. Isolated splenocytes from the immunized mice were fused with an aminopterin-sensitive mouse myeloma cell line, SP2/0-Ag14, to produce hybridoma cells that secreted a monoclonal antibody (MAb) against AA-II. The selected hybridoma was subsequently cloned by limited dilution method. For MAb, the isotype and an estimated dissociation constant (K_D) of the MAb were determined. The MAb was used to establish an ELISA method. Accuracy and variation assays, as well as determinations of the specificity and sensitivity, were also carried out and the linear range was 0.19–13 μg/ml. The anti-AA-II MAb showed a very high specificity for AA-II and had low cross-reactivities against the other aristolochic acid (AAs) (CR: AA-I, 3.4%; AA-VIIa, 0.86%) or aristololactam-I (AL-I) (CR < 0.07%) except AA-IIIa which has 17% of cross activity. Anti-AA-II MAb also showed negligible cross-reactivity (< 0.5%) toward other natural compounds with different chemical structures including barbaloin, sennoside A, rutin, glycyrrhizin, caffeic acid etc. This is the first time that an ELISA method was successfully established for the application of anti-AA-II MAb.