Sulforaphane controls the release of paracrine factors by keratinocytes and thus mitigates particulate matter-induced premature skin aging by suppressing melanogenesis and maintaining collagen homeostasis.

BACKGROUND: Skin aging, potentially caused by exposure to particulate matter (PM)2.5, is characterized by wrinkling, abnormal pigmentation, and skin dryness triggered by several keratinocyte-derived paracrine factors. Sulforaphane (4-methylsulfinylbutyl isothiocyanate, SFN), commonly found in cruciferous vegetables, has diverse biological effects on skin tissue. PURPOSE: In the present study, we have investigated whether SFN may alleviate PM2.5-induced premature skin aging. METHODS: We used keratinocyte/melanocyte or keratinocyte/fibroblast coculture models of skin cells and measured the parameters of melanogenesis, collagen homeostasis and inflammation. RESULTS: SFN inhibited the development of reactive oxygen species in keratinocytes exposed to PM2.5. In keratinocyte/melanocyte cocultures, it significantly inhibited the upregulation of melanogenic paracrine mediators (including endothelin-1 and prostaglandin E2) in keratinocytes exposed to PM2.5; the synthesis of melanogenic proteins including microphthalmia-associated transcription factor, tyrosinase-related protein 1, and tyrosinase; and the levels of melanin in melanocytes. SFN treatment of keratinocyte/fibroblast cocultures significantly reduced the PM2.5-induced expression of NF-κB-mediated cytokines including interleukin-1ß, interleukin-6, tumor necrosis factor α, and cyclooxygenase-2. In fibroblasts of the keratinocyte/fibroblast coculture system, the expression levels of phospho-NF-κB, cysteine-rich protein 61, and matrix metalloproteinase-1 were significantly decreased whereas procollagen type I synthesis was significantly increased. CONCLUSION: Collectively, our results suggest that SFN mitigates PM2.5-induced premature skin aging by suppressing melanogenesis and maintaining collagen homeostasis. It acts by regulating the release of paracrine factors from keratinocytes.

Alpha-Linolenic Acid Alleviates Dextran Sulfate Sodium-Induced Ulcerative Colitis in Mice.

Ulcerative colitis (UC) is a type of inflammatory bowel disease characterized by inflammation of the large intestine, rectal bleeding, and abdominal pain. It can be alleviated by certain bioactive compounds, including α-linolenic acid (ALA), which is a bioactive component in fermented black radish (Raphanus sativus L. var. niger). The aim of this study was to evaluate the anti-inflammatory effects of ALA in dextran sulfate sodium (DSS)-induced UC in mice. UC was induced in C57BL/6 mice by allowing them to freely drink water containing 2.5% DSS for 7 days, followed by oral administration of ALA (30 and 60 mg/kg/day) or vehicle control for 7 days. DSS-induced colitis was evaluated using the Disease Activity Index (DAI) and by measuring colon length and performing a histopathological examination. Compared to the control group, the vehicle-treated group showed a higher DAI score, shorter colon, goblet cell loss, and crypt shortening. The ALA treatment mitigated clinical signs of UC and histopathological changes. Furthermore, it mitigated intestinal inflammation by reducing the expression of ionized calcium binding adaptor molecule 1-positive macrophages in the colon. These results show that ALA alleviates DSS-induced UC by suppressing colon damage, which includes goblet cell loss, crypt shortening, and a reduction of macrophages in the colon.

Fermented black radish (Raphanus sativus L. var. niger) attenuates methionine and choline deficient diet-induced nonalcoholic fatty liver disease in mice.

As one of the wide-ranging form of chronic liver disease, there are only limited therapeutic options for nonalcoholic fatty liver disease (NAFLD). We evaluated whether fermented black radish (Raphanus sativus L. var. niger; FBR) ameliorates lipid accumulation, inflammation, and hepatic fibrosis, which are characteristics of the pathogenesis of NAFLD. Fermented black radish treatment reduced lipid accumulation in 3T3-L1 adipocytes, which appeared to be associated with the downregulation of adipogenic transcription factors, including sterol regulatory element-binding protein 1c, CCAAT/enhancer-binding protein α, peroxisome proliferator-activated receptor γ, and lipid accumulation-related genes including adipocyte protein-2 and fatty acid synthase. Administration of FBR to C57BL/6J mice challenged with methionine and choline deficient (MCD) diet significantly attenuated the increased serum levels of alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and triglyceride. In addition, treatment with FBR interestingly repressed the hepatic inflammation induced with MCD diet, by lowering the expression of inducible nitric oxide synthase and suppressing the inactivation of macrophages and Kupffer cells in the liver. Fermented black radish was also shown to mitigate liver fibrosis through the inhibition of alpha-smooth muscle actin, transforming growth factor beta-1, and collagen type I alpha 1 chain. Our results indicate that FBR ameliorates NAFLD and its related metabolic disease by regulating multiple pathways, suggesting that FBR may be an effective dietary supplement for ameliorating NAFLD.

Black Radish (Raphanus sativus L. var. niger) Extract Mediates Its Hepatoprotective Effect on Carbon Tetrachloride-Induced Hepatic Injury by Attenuating Oxidative Stress.

Nonalcoholic fatty liver disease is a serious liver disorder associated with oxidative stress. Black radish (Raphanus sativus L. var. niger) extract (BRE) can lower the risk of this disease. The hepatoprotective effect of BRE containing 3-(E)-(methylthio)methylene-2-pyrrolidinethione was evaluated in human hepatocyte carcinoma (HepG2) cells and in rat livers with carbon tetrachloride (CCl4)-induced hepatic injury. BRE was administered at 125, 250, 500, and 1000 µg/mL to the oleic acid-induced HepG2 cells. Male Sprague-Dawley rats were randomly divided into seven groups: the control group, BRE group, CCl4 group, and BRE + CCl4 group. BRE was administered orally at 125, 250, 500, and 1000 mg/kg/day once daily for 7 consecutive days, followed by a single oral treatment of 1.5 mL/kg CCl4. Inhibition of lipid accumulation, serum markers of liver injury, histological evaluations, levels of oxidative stress related enzymatic and nonenzymatic antioxidants in HepG2 cells and liver tissue were investigated. The protein expression of main liver P450 isoenzymes such as cytochrome p450(CYP)2E1, the expression of nuclear factor erythroid 2-related factor-2(Nrf-2) and heme oxygenase-1(HO-1) were also studied. BRE has an inhibitory effect on lipid accumulation and caused acute hepatotoxicity manifested by increased levels of lipid peroxidation, serum alanine aminotransferase, and aspartate aminotransferase with corresponding histopathological changes and high levels of oxidative stress. BRE treatment significantly increased the level of CYP2E1, Nrf-2, and HO-1 in a dose-dependent manner. Besides, 3-(E)-(methylthio)methylene-2-pyrrolidinethione significantly increased radical-scavenging effects and the expression of Nrf-2 in oleic acid-treated HepG2 cells. These results suggest that BRE treatment reduces lipid accumulation in oleic acid-induced steatosis of HepG2 cells, and has a hepatoprotective effect against CCl4-induced liver injury in rats, possibly through Nrf-2/HO-1-mediated antioxidant effects.

Neuropharmacological Potential of Gastrodia elata Blume and Its Components.

Research has been conducted in various fields in an attempt to develop new therapeutic agents for incurable neurodegenerative diseases. Gastrodia elata Blume (GE), a traditional herbal medicine, has been used in neurological disorders as an anticonvulsant, analgesic, and sedative medication. Several neurodegenerative models are characterized by oxidative stress and inflammation in the brain, which lead to cell death via multiple extracellular and intracellular signaling pathways. The blockade of certain signaling cascades may represent a compensatory therapy for injured brain tissue. Antioxidative and anti-inflammatory compounds isolated from natural resources have been investigated, as have various synthetic chemicals. Specifically, GE rhizome extract and its components have been shown to protect neuronal cells and recover brain function in various preclinical brain injury models by inhibiting oxidative stress and inflammatory responses. The present review discusses the neuroprotective potential of GE and its components and the related mechanisms; we also provide possible preventive and therapeutic strategies for neurodegenerative disorders using herbal resources.

Hepatoprotective effects of Lycium chinense Miller fruit and its constituent betaine in CCl4-induced hepatic damage in rats.

The hepatoprotective activities of Lycium chinense Miller (LC) fruit extract and its component betaine were investigated under carbon tetrachloride (CCl4)-induced hepatotoxicity in rats. The treatment of LC fruit extract significantly suppressed the increase of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in the sera of CCl4 injured rats, and restored the decreased levels of anti-oxidant enzymes such as total antioxidant capacity (TAC), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) and suppressed the expression of inflammatory mediators including inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-1 and -2. To visualize the potential activity of betaine, a component of LC fruit, betaine was substituted for LC extract in CCl4 injured rats. The biochemical profile in CCl4 injured rats co-treated with betaine matched those of LC fruit treated CCl4 injured rats. The ameliorative effects of LC extract, as well as betaine, were also confirmed by histopathological examination. Collectively, the present findings imply that LC fruit, via its component betaine, mitigate CCl4-induced hepatic injury by increasing antioxidative activity and decreasing inflammatory mediators including iNOS and COX-1/COX-2.

Impact of acupuncture by using life-energy (qi) oriental needle on the paralysis of rats with experimental autoimmune encephalomyelitis.

In acupuncture, adaptation to energy flows in body cycles is the key to health and therapy. From the evolution of our thinking about acupuncture, we developed the Life-Energy (Qi) oriental needle (Qi needle). It contains a rotating electromagnetic wave and has a strong affinity for the meridians. We report for the first time on the effect of acupuncture by using a Qi needle (Qi acupuncture) on rat experimental autoimmune encephalomyelitis, a model of human demyelinating multiple sclerosis. Both Qi acupuncture (QA) and general acupuncture (GA) were used on the limbs, at the shaoshang (LU11) and zhongchong (PC9) acupoints, of rats from one day post-immunization (dpi) to 12 dpi. The therapy in the QA groups significantly blocked the onset of EAE paralysis (3/13, 77%, p < 0.05) while all rats in the control EAE groups (12/15) and GA groups (11/13) showed EAE paralysis. In addition, the duration of paralysis was shortened in QA groups (1.5 ± 0.5 days) compared with those of the vehicle (5.5 ± 0.2 days) and GA groups (3.6 ± 1.1 days). The numbers of inflammatory cells and CD4(+) T cells in the QA treated EAE group were significantly reduced compared with those of the EAE control and EAE with GA (p < 0.05). Collectively, the present findings suggest that QA ameliorates the paralysis in rats in an EAE model. The precise mechanism of the amelioration and human studies, however, needs further study.

Eutigoside C attenuates radiation-induced crypt injury in the mouse intestine.

On Jeju Island, South Korea, the leaves of Eurya emarginata have been traditionally used to treat ulcers or as a diuretic. Eutigoside C isolated from the leaves has been reported to have in vitro anti-inflammatory effects. We evaluated the radioprotective effects of eutigoside C on jejunal cell apoptosis and crypt survival in mice subjected to gamma irradiation. In addition, the ability of eutigoside C to protect against radiation-induced oxidative stress was examined by evaluating the activities of superoxide dismutase (SOD) and catalase (CAT) in radiation-induced hepatic injury. Eutigoside C was administered intraperitoneally at 48, 12, and 1 h before irradiation. The administration of eutigoside C (10, 50, or 100 mg/kg body weight) before irradiation protected the intestinal crypts from radiation-induced apoptosis (p < 0.05), and attenuated radiation-induced decrease of villous height (p < 0.05). Pretreating mice prior to irradiation with eutigoside C (100 mg/kg) significantly improved the survival of the jejunal crypt (p < 0.01). The dose reduction factor was 1.09 at 3.5 days after irradiation. Treatment of eutigoside C prior to irradiation significantly protected SOD and CAT activities in radiation-induced hepatic injury (p < 0.05). These results suggest that eutigoside C is a useful radioprotector capable of defending intestinal progenitor cells against indirect depletion, such as oxidative stress and inflammatory response caused by gamma irradiation.

Amelioration of experimental autoimmune encephalomyelitis in Lewis rats treated with fucoidan.

We examined whether fucoidan affected the clinical symptoms of experimental autoimmune encephalomyelitis (EAE) in rats. EAE was induced in Lewis rats that were immunized with guinea-pig myelin basic protein (MBP) and complete Freund's adjuvant. Fucoidan (50 mg/kg, daily) was administered to rats with EAE intraperitoneally, either in the EAE induction phase from either 1 day before immunization to day 7 post-immunization (PI), or the effector phase from day 8 to 14 PI, to test which phase of rat EAE is affected by fucoidan treatment.The onset, severity and duration of EAE paralysis in the fucoidan-treated group in the days 8-14 PI-treated rats, but not in days -1-7 PI-treated rats, were significantly delayed, suppressed and reduced, respectively, compared with the vehicle-treated controls. Treatment with fucoidan reduced the encephalitogenic response and TNF-alpha production during EAE. Moreover, the clinical amelioration coincided with decreased infiltration of inflammatory cells in the EAE-affected spinal cord. The ameliorative effect of fucoidan on clinical paralysis in EAE-affected rats may be mediated, in part, by the suppression of the autoreactive T cell response and inflammatory cytokine production.

Radioprotective effects of fucoidan in mice treated with total body irradiation.

The effects of fucoidan on the survival rate of mice treated with total body irradiation were examined. BALB/c mice were pretreated with various doses of fucoidan prior to total-body irradiation and were monitored for 30 days. A significant improvement of survival was observed by pretreatment with fucoidan at 100 mg/kg body weight. Using this optimal dosage, survival was examined by radiation dose reduction analysis and a dose reduction factor (DRF) of 1.20 was determined at 30 days post-irradiation. Mice pretreated with fucoidan also exhibited dose-dependent increases in the number of bone marrow cells and endogenous spleen cell colonies at day 9 post-irradiation. It is concluded that the increased survival of whole-body irradiated mice pretreated with fucoidan may be attributable to the radioprotective effects of fucoidan on hematopoietic cell viability, proliferation and/or mobility, possibly through antioxidation or antiinflammatory mechanisms.

The radioprotective effects of the hexane and ethyl acetate extracts of Callophyllis japonica in mice that undergo whole body irradiation.

The radioprotective activity of extracts from the red seaweed Callophyllis (C.) japonica was investigated in mice that underwent whole-body exposure to gamma radiation. A methanol extract of C. japonica and its fractions [hexane, ethyl acetate (EtOAc), butanol and the remaining H2O] were used. Each fraction (100 mg/kg body weight) was administered intraperitoneally (i.p.) 2 times into the BALB/c mice, once at 1 and once at 24 h before exposure to 9 Gray (Gy) of gamma radiation. Pre-irradiation administration of the hexane and EtOAc fractions saved the mice, with their survival rates being greater than 80% at 30 days post-irradiation; the mice that were pretreated with the other fractions showed survival rates lower than 20% over the same time period. To examine the effect of each C. japonica fraction on the survival of intestinal and bone marrow stem cells, the number of intestinal crypts and bone marrow cells in the gamma-irradiated mice were examined. Pre-treatment of mice (i.p., 100 mg/kg body weight at 1 and 24 h before irradiation) with the hexane or EtOAc fraction prior to 6-Gy irradiation significantly protected the number of jejunal crypts and bone marrow cells at 9 days after irradiation. These findings suggest that certain extracts from C. japonica, when they are administered prior to irradiation, play an important role in the survival of irradiated mice, and this is possibly due to the extracts protecting the hematopoietic cells and intestinal stem cells against gamma irradiation.

Protective effect of phlorotannin components phloroglucinol and eckol on radiation-induced intestinal injury in mice.

Components of phlorotannin, which were extracted from Ecklonia species, have been reported to have in vitro radioprotective and antioxidative effects. The radioprotective effects of two of the components of phlorotannin, phloroglucinol and eckol, in intestinal stem cells were examined by evaluating their effects on jejunal crypt survival and apoptosis in gamma-irradiated mice. Pretreating the mice (i.p. 20 mg/kg of body weight at 12 and 36 h before irradiation) prior to irradiation with either phloroglucinol or eckol significantly improved the survival of the jejunal crypt (p < 0.001 and p < 0.01 vs irradiation controls at 3.5 days after 8 Gy irradiation, respectively). The administration of phloroglucinol and eckol prior to irradiation protected the intestinal crypts from radiation-induced apoptosis (p < 0.05 vs irradiation controls at 12 h after 1 Gy irradiation). Although the mechanism for this inhibitory effect remains unknown, these results showed that phloroglucinol and eckol might be useful radioprotectors that can defend intestinal stem cells against the oxidative damage caused by gamma-irradiation.

Opuntia ficus-indica attenuates neuronal injury in in vitro and in vivo models of cerebral ischemia.

We examined whether the methanol extract of Opuntia ficus-indica (MEOF) has a neuroprotective action against N-methyl-d-aspartate (NMDA)-, kainate (KA)-, and oxygen-glucose deprivation (OGD)-induced neuronal injury in cultured mouse cortical cells. We also evaluated the protective effect of MEOF in the hippocampal CA1 region against neuronal damage evoked by global ischemia in gerbils. Treatment of neuronal cultures with MEOF (30, 300, and 1000 microg/ml) inhibited NMDA (25 microM)-, KA (30 microM)-, and OGD (50 min)-induced neurotoxicity dose-dependently. The butanol fraction of Opuntia ficus-indica (300 microg/ml) significantly reduced NMDA (20 microM)-induced delayed neurotoxicity by 27%. Gerbils were treated with MEOF every 24h for 3 days (0.1, 1.0, and 4.0 g/kg, p.o.) or for 4 weeks (0.1 and 1.0 g/kg, p.o.), and ischemic injury was induced after the last dose. Neuronal cell damage in the hippocampal CA1 region was evaluated quantitatively at 5 days after the ischemic injury. When gerbils were given doses of 4.0 g/kg (3 days) and 1.0 g/kg (4 weeks), the neuronal damage in the hippocampal region was reduced by 32 and 36%, respectively. These results suggest that the preventive administration of Opuntia ficus-indica extracts may be helpful in alleviating the excitotoxic neuronal damage induced by global ischemia.

Association between tumor necrosis factor-alpha gene polymorphism and Sasang constitution in cerebral infarction.

During the last decade, a growing corpus of evidence has indicated an important role of cytokines in the development of brain damage following cerebral ischemia. Tumor necrosis factor-alpha (TNF-alpha), a potent immunomodulator and pro-inflammatory cytokine, has been implicated in many pathological processes. In this study, we examined whether promoter region polymorphism in the TNF-alpha gene at position -308 affects the odds of cerebral infarction (CI) and whether genetic risk is enhanced by Sasang constitutional classification. Two hundred and twelve CI patients and 610 healthy controls were genotyped and determined according to Sasang constitutional classification. A significant decrease was found for the TNF-alpha A allele in CI patients compared with controls (p = 0.033, odds ratio, OR: 0.622). However, there was no significant association between TNF-alpha polymorphism and Sasang constitution in CI patients. Our finding suggests that TNF-alpha promoter region polymorphism is responsible for susceptibility to CI in Koreans.

Antioxidant activity of ethanol extract of Callophyllis japonica.

The antioxidant properties of the red seaweed Callophyllis japonica were investigated. An ethanol extract isolated from C. japonica exhibited intracellular reactive oxygen species, 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical scavenging activity and lipid peroxidation inhibitory activity. The radical scavenging activity of the extract protected the viability of Chinese hamster lung fibroblast (V79-4) cells exposed to H2O2. Furthermore, the extract reduced the proportion of apoptotic cells induced by H2O2, as demonstrated by decreased sub-G1 hypo-diploid cells and decreased apoptotic body formation. The extract also increased the activities of the cellular antioxidant enzymes, superoxide dismutase and catalase. Together, these findings suggest that C. japonica exhibits antioxidant properties.

Hypoxia-induced IL-6 production is associated with activation of MAP kinase, HIF-1, and NF-kappaB on HEI-OC1 cells.

In the present study, we investigated the signal transduction pathways of expression of IL-6 in the desferrioxamine (DFX)-stimulated cochlear auditory cell line, HEI-OC1 cells. DFX increased the expression of HIF-1alpha and NF-kappaB in HEI-OC1 cells. DFX significantly increased the production of IL-6 (P<0.05) and expression of IL-6 mRNA but did not affect TNF-alpha production. DFX also induced the activation of mitogen-activated protein kinase (MAPK) including p38, ERK, and JNK on HEI-OC1. Increased IL-6 by DFX was significantly inhibited by p38 inhibitor, SB203580 (about 72% inhibition, P=0.027) but not ERK inhibitor, PD98059 or JNK inhibitor, SP600125. SB203580 inhibited the expression of IL-6 mRNA. Increased IL-6 production was partially inhibited by treatment of iron (HIF-1 inhibitor) or pyrriolidine-dithiocarbamate (PDTC, NF-kappaB inhibitor). DFX also induced IL-6 production and HIF-1alpha expression in the inner ear. We demonstrated the regulatory effects of MAPK, HIF-1alpha, and NF-kappaB on DFX-induced IL-6 production in a HEI-OC1 for the first time. In conclusion, these data indicate that regulation of inflammatory cytokine IL-6 by DFX, through mimicking hypoxic conditions, might explain its beneficial effect in the treatment of hypoxia-induced inner ear diseases.

Regulatory effect of atopic allergic reaction by Carpopeltis affinis.

Carpopeltis affinis Okamura (CA, Halymeniaceae) has long been used as therapeutics for various allergic diseases in Korea. The precise effects of CA in experimental models, however, have remained unknown. We studied the effects of a methanol extract of CA on atopic allergic reaction. Histamine content was measured by the o-phthalaldehyde spectrofluorometric procedure. Cytokines were measured by a modified enzyme-linked immunosorbent assay. Cytotoxicity was determined by the 3-(4,5-dimethythiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT) assay. CA significantly inhibited the histamine release and beta-hexosaminidase release from rat peritoneal mast cells. CA also inhibited interleukin-8 and tumor necrosis factor-alpha secretion from the phorbol 12-myristate 13-acetate and A23187-induced HMC-1 cells (human mast cell line). 48 h exposure to CA (1.0, 10, and 100 microg/ml) had little effect on HMC-1 cell viability. Our results suggest that CA has an inhibitory effect on mast cell-dependent allergic reaction and thus may be useful in the treatment of atopic dermatitis.

Reductive effect of body weight in C57BL/6J mice fed a high-fat diet by Saesaengmyung Diet.

The Saesaengmyung Diet (SD) is a newly developed dietary product to help control weight. The aim of this study was to evaluate whether SD combined with a high-fat (HF) diet could influence body weight, fat accumulation, and glucose levels in blood. C57BL/6J mice were fed for 8 weeks with a standard diet, an HF diet, and an HF + 10% or HF + 20% SD diet. Body weight was recorded weekly, and plasma levels of total cholesterol, low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, and glucose were analyzed at the end of the study. Weight increases in the 10% or 20% SD group were significantly less than in the HF diet group (p < 0.05). Plasma total cholesterol level significantly decreased by 33.5% in the 10% SD group and 38.8% in the 20% SD group, but the LDL cholesterol, HDL cholesterol, and glucose levels in the SD groups were not significantly changed. Our findings indicate that SD may be beneficial to overweight individuals in the reduction of weight gain induced by an HF diet.

An herbal formula, Herbkines, enhances cytokines production from immune cells.

Herbkines is a newly modified Oriental drug prescription for the purpose of immune enhancement, especially for those who are suffered from wasting diseases like cancer in Korea. In the present study, Herbkines has been applied to human leukemic T-cell lines (MOLT-4) and cytokines were estimated by enzyme linked immuno-sorbent assay (ELISA) to assess the effects of Herbkines on cytokines production. Interferon-gamma production was increased by about five-folds at the dose of 1 mg/ml compared to control when Herbkines was applied to a T cells, MOLT-4. Interleukin (IL)-4 production showed high variation in dependence with doses. IL-2 production was increased by about three-folds at the Herbkines dose of 0.1 mg/ml. In addition, Herbkines increased the production of tumor necrosis factor-alpha and IL-12 on the mouse peritoneal macrophages (by 7.3-fold for TNF-alpha and 2.2-fold for IL-12, respectively). These data suggest Herbkines has immune-enhancement effect through the cytokine production.

Differential regulation by Seogak Jihwang-Tang on cytokines production in peripheral blood mononuclear cells from the cerebral infarction patients presenting with altered consciousness.

Seogak Jihwang-Tang (SJT) has been widely used to treat patients suffering from cerebral infarction. However, very little scientific investigation has been carried out. We investigated the effect of SJT on the production of various cytokines using peripheral blood mononuclear cells from the cerebral infarction patients presenting with altered consciousness. The cytokines production was determined by enzyme-linked immunosorbent assay. The amount of IL-4, IL-10 and TGF-beta1 in culture supernatant significantly increased in the SJT, lipopolysaccharide (LPS) or PHA-treated cells compared to unstimulated cells (P < 0.05). We also showed that increased IL-4 and IL-10 levels by LPS or phytohaemagglutinin (PHA) were significantly inhibited by SJT in a dose-dependent manner. Maximal inhibition rate of IL-4 and IL-10 production by SJT was 45.6 +/- 3.3% and 61 +/- 4.7% for LPS-stimulated cells and 27.3 +/- 1.2% and 83.6 +/- 2% for PHA-stimulated cells, respectively (P < 0.05). On the other hand, SJT significantly increased the LPS or PHA-induced TGF-beta1 production (P < 0.05). These data suggest that SJT has a regulatory effect on the cytokines production, which might explain its beneficial effect in the treatment of cerebral infarction.