Vasorelaxant and Blood Pressure-Lowering Effects of Cnidium monnieri Fruit Ethanol Extract in Sprague Dawley and Spontaneously Hypertensive Rats.

Cnidium monnieri (L.) Cusson, a member of the Apiaceae family, is rich in coumarins, such as imperatorin and osthole. Cnidium monnieri fruit (CM) has a broad range of therapeutic potential that can be used in anti-bacterial, anti-cancer, and sexual dysfunction treatments. However, its efficacy in lowering blood pressure through vasodilation remains unknown. This study aimed to assess the potential therapeutic effect of CM 50% ethanol extract (CME) on hypertension and the mechanism of its vasorelaxant effect. CME (1-30 µg/mL) showed a concentration-dependent vasorelaxation on constricted aortic rings in Sprague Dawley rats induced by phenylephrine via an endothelium-independent mechanism. The vasorelaxant effect of CME was inhibited by blockers of voltage-dependent and Ca2+-activated K+ channels. Additionally, CME inhibited the vascular contraction induced by angiotensin II and CaCl2. The main active compounds of CM, i.e., imperatorin (3-300 µM) and osthole (1-100 µM), showed a concentration-dependent vasorelaxation effect, with half-maximal effective concentration values of 9.14 ± 0.06 and 5.98 ± 0.06 µM, respectively. Orally administered CME significantly reduced the blood pressure of spontaneously hypertensive rats. Our research shows that CME is a promising treatment option for hypertension. However, further studies are required to fully elucidate its therapeutic potential.

Proximal Junctional Kyphosis or Failure After Adult Spinal Deformity Surgery - Review of Risk Factors and Its Prevention.

Proximal junction kyphosis (PJK) is a common imaging finding after long-level fusion, and proximal junctional failure (PJF) is an aggravated form of the progressive disease spectrum of PJK. This includes vertebral fracture of upper instrumented vertebra (UIV) or UIV+1, instability between UIV and UIV+1, neurological deterioration requiring surgery. Many studies have reported on PJK and PJF after long segment instrumentation for adult spinal deformity (ASD). In particular, for spine deformity surgeons, risk factors and prevention strategies of PJK and PJF are very important to minimize reoperation. Therefore, this review aims to help reduce the occurrence of PJK and PJF by updating the latest contents of PJK and PJF by 2023, focusing on the risk factors and prevention strategies of PJK and PJF. We conducted a search on multiple database for articles published until February 2023 using the search keywords "proximal junctional kyphosis," "proximal junctional failure," "proximal junctional disease," and "adult spinal deformity." Finally, 103 papers were included in this study. Numerous factors have been suggested as potential risks for the development of PJK and PJF, including a high body mass index, inadequate postoperative sagittal balance and overcorrection, advanced age, pelvic instrumentation, and osteoporosis. Recently, with the increasing elderly population, sarcopenia has been emphasized. The quality and quantity of muscle in the surgical site have been suggested as new risk factor. Therefore, spine surgeon should understand the pathophysiology of PJK and PJF, as well as individual risk factors, in order to develop appropriate prevention strategies for each patient.

Davidone C Induces the Death of Hepatocellular Carcinoma Cells by Promoting Apoptosis and Autophagy.

Davidone C is a newly discovered flavonoid compound purified from the ethyl acetate-soluble fraction of Sophora davidii (Franch.) Skeels. This study explored the anti-tumor activity of davidone C on hepatocellular carcinoma HepG2 and Bel-7402 cells and its mechanism through MTT method, morphological observation, flow cytometry and Western blotting. The results showed that davidone C significantly inhibited the proliferation of HepG2 and Bel-7402 cells in a time- and dose-dependent manner. The morphological changes of apoptotic cells can be observed under an inverted microscope, such as cell floating, chromosome condensation, apoptotic bodies, and other phenomena. The expressions of Bax, cleaved caspase-9, cleaved caspase-3 and cleaved PARP increased with the increase of dosage while Bcl-2 decreased, suggesting that the apoptotic mechanism might be related to the mitochondrial apoptotic pathway. Moreover, davidone C administration can down-regulate the expression of Grp78, and simultaneously up-regulate the expression of caspase-7 and caspase-12, indicating that the apoptotic mechanism might be related to the ERS pathway. In addition, davidone C can down-regulate the expression of p62, and simultaneously up-regulate the expression of LC3-I and LC3-II with a quantitative dependence, suggesting that the mechanism of apoptosis may be related to the autophagy signal pathway. All these results showed davidone C has potential effects on hepatocellular carcinoma.

Anti-esophageal Cancer Effect of Corilagin Extracted from Phmllanthi Fructus via the Mitochondrial and Endoplasmic Reticulum Stress Pathways.

HEADINGS ETHNOPHARMACOLOGICAL RELEVANCE: Corilagin (ß-1-O-galloyl-3,6-(R)-hexahydroxydiphenoyl-d-glucose) is a tannin isolated from the traditional ethnopharmacological plant Phmllanthi Fructus, which is widely used in not only traditional Chinese medicine but also tropical and subtropical medicine to ameliorate various diseases. AIM OF THE STUDY: This study was designed to isolate the potential anti-esophageal cancer (EC) component corilagin from Phmllanthi Fructus and explain its anti-EC mechanism. MATERIALS AND METHODS: Corilagin was isolated from Phmllanthi Fructus by extraction and chromatographic procedures, and its anti-esophageal cancer effect was evaluated by in vitro and in vivo experiments. In vitro experiments included MTT analysis, flow cytometry, and the Transwell assay and were used to observe corilagin-mediated inhibition of EC cell growth. Western blotting was used to analyze the apoptotic pathway of EC cells. In vivo experiments used tumor-bearing nude mice to evaluate the antitumor effect of corilagin, and its potential mechanism was explored by Western blotting. RESULTS: Corilagin showed significant anti-EC activity in vitro and in vivo. Corilagin was significantly cytotoxic to EC cells and induced apoptosis in EC cells. Corilagin induced G0/G1 phase arrest by altering key G0/G1 cell cycle regulatory markers and significantly reducing the migration of EC cells and the number of cells in a time- and dose-dependent manner. Additionally, corilagin inhibited the growth of transplanted tumors in nude mice without significant toxicity. Regarding the anticancer mechanism of corilagin, the results showed that corilagin inhibited esophageal cancer progression by activating mitochondrial and endoplasmic reticulum stress signaling pathways. CONCLUSIONS: Corilagin shows significant anti-EC activity in vitro and in vivo. The mechanism of the anti-EC activity of corilagin may be due to activating mitochondrial and endoplasmic reticulum stress signaling pathways.

Endothelium-Dependent Vasorelaxant Effect of Prunus Persica Branch on Isolated Rat Thoracic Aorta.

Peach (Prunus persica (L.) Batsch) is a popular fruit consumed by people worldwide, owing to its pleasant flavor and high mineral nutrient content. A few plants from the genus Prunus, such as Prunus yedoensis, Prunus cerasus, and Prunus serotina have shown vasorelaxant and vasodilatory effects, to date, no study has investigated the vasorelaxation effects of the P. persica branch extract (PPE). The vasorelaxant effect of PPE was endothelium-dependent, and it was related to the NO-sGC-cGMP, vascular prostacyclin, and muscarinic receptor transduction pathway. K+ channels, such as the BKCa, KV, and KATP channels, were partially associated with PPE-induced vasorelaxation. PPE was effective in relaxing serotonin (5-HT)- or angiotensin II-induced contraction; furthermore, PPE attenuated Ca2+-induced vasoconstriction by IP3 receptors in the SR membrane, but its vasorelaxant effect was not associated with the influx of extracellular Ca2+ via receptor-operative Ca2+ channels or voltage-dependent Ca2+ channels. Recognizing the rising use of functional foods for hypertension treatment, our findings imply that PPE may be a natural antihypertensive agent.

HVC1 ameliorates hyperlipidemia and inflammation in LDLR-/- mice.

BACKGROUND: HVC1 consists of Coptidis Rhizoma (dried rhizome of Coptischinensis), Scutellariae Radix (root of Scutellariabaicalensis), Rhei Rhizoma (rhizome of Rheum officinale), and Pruni Cortex (cortex of Prunusyedoensis Matsum). Although the components are known to be effective in various conditions such as inflammation, hypertension, and hypercholesterolemia, there are no reports of the molecular mechanism of its hypolipidemic effects. METHODS: We investigated the hypolipidemic effect of HVC1 in low-density lipoprotein receptor-deficient (LDLR-/-) mice fed a high-cholesterol diet for 13 weeks. Mice were randomized in to 6 groups: ND (normal diet) group, HCD (high-cholesterol diet) group, and treatment groups fed HCD and treated with simvastatin (10 mg/kg, p.o.) or HVC1 (10, 50, or 250 mg/kg, p.o.). RESULTS: HVC1 regulated the levels of total cholesterol, triglyceride (TG), low-density lipoprotein (LDL) cholesterol, and high-density lipoprotein (HDL) cholesterol in mouse serum. In addition, it regulated the transcription level of the peroxisome proliferator-activated receptors (PPARs), sterol regulatory element-binding proteins (SREBP)-2, 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase, lipoprotein lipase (LPL), apolipoprotein B (apo B), liver X receptor (LXR), and inflammatory cytokines (IL-1ß, IL-6, and TNF-α). Furthermore, HVC1 activated 5' adenosine monophosphate-activated protein kinase (AMPK). CONCLUSION: Our results suggest that HVC1 might be effective in preventing high-cholesterol diet-induced hyperlipidemia by regulating the genes involved in cholesterol and lipid metabolism, and inflammatory responses.

Hypolipidemic effects of HVC1 in a high cholesterol diet­induced rat model of hyperlipidemia.

HVC1, a novel formation containing four herbs, was developed and its hypolipidemic effects in rats with high cholesterol diet (HCD)­induced hyperlipidemia were investigated. The rats were given a HCD for 8 weeks. The HVC1­treated groups were orally administered HVC1 at doses of 10, 50 or 250 mg/kg, respectively, and the simvastatin group was treated at a dose of 10 mg/kg. The normal diet and HCD control groups were administered with physiological saline. Oral administration of HVC1 (10, 50 or 250 mg/kg) significantly reduced the body weight of rats with hyperlipidemia and regulated the total cholesterol, low­density lipoprotein cholesterol and high­density lipoprotein cholesterol levels in the serum. In addition, tissue analysis revealed that lipid accumulation in the liver and aorta was reduced by HVC1 administration. Furthermore, HVC1 significantly reduced the mRNA expression of peroxisome proliferator­activated receptor­Î³, 3­hydroxy­3­methylglutaryl­CoA reductase and low­density lipoprotein receptor, as well as the protein level of 5' adenosine monophosphate­activated protein kinase in the liver. The results clearly demonstrate that HVC1 has a potent hypolipidemic effect, and suggest that HVC1 should be evaluated as a potential treatment for hyperlipidemia.

Effect of Acer tegmentosum bark on atopic dermatitis-like skin lesions in NC/Nga mice.

ETHNOPHARMACOLOGICAL RELEVANCE: Atopic dermatitis (AD) is a chronic and relapsing inflammatory condition characterized by pruritic and eczematous skin lesions that requires safe and effective pharmacological therapy. The bark of Acer tegmentosum Maxim trees has been used in Korean folk and traditional medicine to treat abscesses, surgical bleeding, liver diseases, and AD. AIM OF STUDY: To investigate the therapeutic effect of A. tegmentosum, on a mouse model of Dermatophagoides farinae (Df)-induced AD. METHODS: Development of AD-like skin lesions was induced by repetitive skin contact with barrier-disrupted backs of NC/Nga mice with Df body ointment, and the effects of A. tegmentosum were evaluated on the basis of histopathological skin assessment results, ear swelling, and cytokine production in the dorsal skin. The component of A. tegmentosum, salidroside, inhibited the production of TSLP in KCMH-1 cells, which indicated that its production could be pharmacologically regulated. RESULTS: Topical application of A. tegmentosum for 1 week after Df body ointment challenge significantly reduced ear swelling and improved dorsal skin lesions. Suppression of dermatitis by combined therapy was accompanied by a decrease in the skin level of Th2 cytokines, such as interleukin (IL)-4, IL-5 and IL-13, plasma levels of thymus and activation-regulated chemokine, and IgE. Induction of thymic stromal lymphopoietin, which leads to a systemic Th2 response, was also reduced in in vivo and in vitro by A. tegmentosum and salidroside. CONCLUSIONS: Our findings suggest that A. tegmentosum treatment has a significant therapeutic effect on Df-induced AD-like skin lesions on NC/Nga mice through inhibition of thymic stromal lymphopoietin and IgE via a mechanism that may inhibit Th2-mediated immune responses. These results suggest that A. tegmentosum and salidroside may be useful tools for the treatment of AD.

Effect of Ampelopsis Radix on wound healing in scalded rats.

BACKGROUND: Ampelopsis Radix has been used as a traditional Korean medicine for the treatment of burns and scalds. However, there has been no scientific research to date on the wound healing properties of Ampelopsis Radix for scald burns. This study aimed to evaluate the healing effect of Ampelopsis japonica root tuber ethanol extract (AJE) on induced cutaneous scald injury in Sprague Dawley (SD) rats. METHODS: Hot water scalds were induced in SD rats, who were then divided into the following 5 groups; 1) control group without treatment, 2) positive control group with 1% Silver sulfadiazine (SSD), 3) Vaseline group, and groups 4) and 5) that used Vaseline containing 5% and 20% AJE, respectively. The ointment was applied topically to the experimental rats, once daily for 21 days, starting at 24 h post induction of the scald injury. Gross examination, measurement of wound size, and histopathological examination were performed. And quantitative measurement of cytokine levels of tumor necrosis factor alpha (TNF-α), interleukin-10 (IL-10), transforming growth factor beta 1 (TGF-ß1), and vascular endothelial growth factor (VEGF) were performed by enzyme-linked immunosorbent assay. RESULTS: Clinical evaluation showed that the AJE and Vaseline groups, rapidly desquamated scab on day 12 post-scalding; in particular, the 20% AJE group achieved the greatest extent of skin recovery. Sizes of scald wound were significantly lower on days 12, 15, 18, and 21 in the AJE treated groups compared to the control groups. Histopathological evaluation showed a well-organized epithelial layer, angiogenesis, tissue granulation and collagen formation with the exception of inflammatory cells in the AJE-treated groups compared to the control groups on day 14, indicating that tissue regeneration had occurred. AJE treatment decreased TNF-α and increased IL-10 levels on days 2 and 14, indicating the anti-inflammatory action of AJE. The AJE groups also showed a decrease in TGF-ß1 levels on day 7 and VEGF on day 14 in the serum of scald inflicted SD rat model. CONCLUSIONS: These results suggest that AJE possesses scald wound healing activity via accelerating the scald wound repair during the inflammation and proliferative phases of the healing process.

Prunus yedoensis bark inhibits lipopolysaccharide-induced inflammatory cytokine synthesis by IκBα degradation and MAPK activation in macrophages.

The bark of Prunus yedoensis is used in antitussive medicines and in oral herbal formulations for inflammatory skin disorders. In the present study, we explored whether P. yedoensis bark extract (PYE) and its solvent partitioned fractions could modulate lipopolysaccharide (LPS)-induced tumor necrosis factor (TNF)-α and interleukin (IL)-6 in vivo and in vitro. In addition, we examined the effect of PYE extract and its fractions on LPS-induced NF-κB and mitogen-activated protein kinase (MAPK) signaling in mouse peritoneal macrophages. Oral treatment of PYE decreased serum levels of TNF-α and IL-6 in LPS injected mice. PYE inhibited LPS-induced TNF-α and IL-6 in macrophages at the transcriptional level and also suppressed LPS-induced IκBα degradation and MAPK activation in vitro. Among the fractions, the chloroform fraction, which contains genistein, naringenin, sakuranetin, prunetin, and amygdalin, showed inhibitory effects at much lower concentrations than the water and ethyl acetate fractions. Taken together, our results indicate that PYE was able to inhibit LPS-induced expression of TNF-α and IL-6, the latter of which was more prominent. The effects of PYE on inflammatory cytokine synthesis may involve modulation of NF-κB and MAPK activation.

Anti-inflammatory effect of Prunus yedoensis through inhibition of nuclear factor-κB in macrophages.

BACKGROUND: Prunus yedoensis (PY) is a traditional anti-allergy and anti-inflammatory herb medicine used in South Korea. However, until date, little is known regarding its mechanism of action. METHODS: In order to elucidate the mechanism of anti-inflammatory effect of PY, the constituents of PY were analysed by high performance liquid chromatography (HPLC), and nitric oxide (NO) and prostaglandin E2 (PGE2) production were measured enzyme-linked immuno sorbent assay (ELISA). The expression levels of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and nuclear factor-κB (NF-κB) were also measured by western blotting in lipopolysaccharide (LPS)-induced RAW 264.7 macrophage cells treated with PY. RESULTS: The results indicate that (50, 100 µg/mL) methanol and ethyl acetate fractionation extracts of PY not only inhibited LPS-mediated NO production and iNOS expression, but also decreased LPS-induced PGE2 production and COX-2 expression. The anti-inflammatory effects of PY were also due to the attenuation of nuclear translocation of NF-κB, as evaluated by the use of anti-p50 on nuclear fractions. LPS-induced nuclear translocation of NF-κB decreased significantly by the methanol extract and ethyl acetate fraction of PY. High performance liquid chromatography (HPLC) analyses revealed that methanol extract and ethyl acetate fraction have similar patterns of retention time and peaks. CONCLUSION: Our results demonstrate that methanol extracts and the ethyl acetate fraction of PY have anti-inflammatory properties, thus emphasizing the potential of PY as a natural health product.

Anti-inflammatory effect of prunetin via the suppression of NF-κB pathway.

Prunetin is an O-methylated isoflavone, which is found in Prunus yedoensis. To date no report has been published on anti-inflammatory activities of prunetin. In the present study, the anti-inflammatory effect of prunetin on LPS-stimulated RAW 264.7 macrophage and LPS-induced septic shock model were investigated. Inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1ß (IL-1ß) expressions were determined by western blot and or realtime-PCR (RT-PCR). To elucidate its underlying mechanism, nuclear factor-kappa B (NF-κb) activation and its downstream pathways were investigated by NF-κB transcription factor assay, reporter gene expression, and western blot. In vivo anti-inflammatory effects of prunetin were evaluated in LPS-induced endotoxemia. Promoter assay revealed that prunetin inhibits LPS-induced nitric oxide and prostaglandin E2 production through the suppression of iNOS and COX-2 at the transcriptional level. In addition, prunetin inhibits NF-κB-dependent inflammatory responses by modulating IκB kinase (IKK)-inhibitor κBα (IκBα)-NF-κB signaling. Consistent with these results, prunetin significantly reduced serum levels of inflammatory cytokines and mortality in mice challenged with lipopolysaccharide. These findings offer a potential mechanism for the anti-inflammatory activity of prunetin.

Terminalia chebula extract protects OGD-R induced PC12 cell death and inhibits lps induced microglia activation.

Terminalia chebula, native to Southeast Asia, is a popular medicinal plant in Ayurveda. It has been previously reported to have strong antioxidant and anti-inflammatory efficacy. In this study, we aimed to investigate if fruit extract from T. chebula might protect neuronal cells against ischemia and related diseases by reduction of oxidative damage and inflammation in rat pheochromocytoma cells (PC12) using in vitro oxygen-glucose deprivation followed by reoxygenation (OGD-R) ischemia and hydrogen peroxide (H2O2) induced cell death. Cell survival was evaluated by a 2-(4,5-dimethylthiazol- 2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Free radical scavenging, lipid peroxidation and nitric oxide inhibition were measured by diphenyl-1-picrylhydrazyl (DPPH), thiobarbituric acid (TBA) and Griess reagent, respectively. We found that T. chebula extract: (1) increases the survival of cells subjected to OGD-R by 68%, and H2O2 by 91.4%; (2) scavenges the DPPH free radical by 96% and decreases malondialdehyde (MDA) levels from 237.0 ± 15.2% to 93.7 ± 2.2%; (3) reduces NO production and death rate of microglia cells stimulated by lipopolysaccharide (LPS). These results suggest that T. chebula extract has the potential as a natural herbal medicine, to protect the cells from ischemic damage and the possible mechanism might be the inhibition of oxidative and inflammatory processes.

The aerial part of Taraxacum coreanum extract has an anti-inflammatory effect on peritoneal macrophages in vitro and increases survival in a mouse model of septic shock.

ETHNOPHARMACOLOGICAL RELEVANCE: Taraxacum coreanum Nakaiis a dandelion native to Korea and is widely consumed as an edible and medicinal herb. The aerial part of Taraxacum coreanum (TC) has been used therapeutically as a diuretic and anti-inflammatory agent, but its mechanism of action has not yet been evaluated. AIM OF THE STUDY: To investigate the anti-inflammatory potential of a Taraxacum coreanum chloroform fraction(TCC) and its mechanisms of action in vitro and in vivo. MATERIALS AND METHODS: Isolated mouse peritoneal macrophages were stimulated in vitro with interferon-γ (IFN-γ) and lipopolysaccharide (LPS) in the presence or absence of TCC. The anti-inflammatory effects of TCC were assessed by measuring nitric oxide (NO) and prostaglandin E2 (PGE2) production, as well as expression of inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), IκBα, phospho-IKK, mitogen-activated protein kinases (MAPKs), and signal transducer and activator of transcription (STAT1). The effects of TCC were tested in vivo by measuring cytokine production and survival in a mouse model of lethal septic shock. And the standard compounds of Taraxacum coreanum were analyzed by HPLC using a C18 column. RESULTS: Treatment of primary macrophages with TCC in vitro significantly inhibited all of the inflammatory parameters measured, including LPS-induced NO and PGE2 production, iNOS and COX-2 expression, IκBα degradation, IKK phosphorylation, and MAPK and STAT1 activation. In a mouse model of LPS-induced septic shock, TCC inhibited the production of tumor necrosis factor (TNF)-α, interleukin (IL)-1ß, and IL-6, and increased survival by 83%.Standard compounds (gallic acid, syringic acid) of Taraxacum coreanum were qualified by HPLC analysis. CONCLUSIONS: TCC possesses potent anti-inflammatory activity in vitro and in vivo, which occurs at least partly through inhibition of proinflammatory signaling and mediator release. These results strongly support the therapeutic potential of TCC as an anti-inflammatory agent in vivo.

Inhibition of lipopolysaccharide-induced nitric oxide and prostaglandin E2 production by chloroform fraction of Cudrania tricuspidata in RAW 264.7 macrophages.

BACKGROUND: Cudrania tricuspidata extract is an important traditional herbal remedy for tumors, inflammation, gastritis, and liver damage and is predominantly used in Korea, China, and Japan. However, the anti-inflammatory effects of the extract have not yet been conclusively proved. METHODS: In this study, we investigated the effects of the CHCl3 fraction (CTC) of a methanol extract of C. tricuspidata on the lipopolysaccharide (LPS)-induced nitric oxide (NO) and prostaglandin E2 (PGE2) production in RAW 264.7 macrophage cells and mouse peritoneal macrophages, and the levels of pro-inflammatory cytokines tumor necrosis factor-α (TNF-α), interleukin (IL)-1ß and IL-6 in RAW 264.7 macrophage cells. RESULTS: We observed that the protein expression levels of inducible NO synthase and COX-2 enzymes were markedly inhibited by CTC in a concentration-dependent manner. In addition, CTC reduced the production of TNF-α, IL-1ß, and IL-6 in the LPS-stimulated RAW 264.7 macrophage cells. CONCLUSIONS: Our results show that the C. tricuspidata extract could modulate macrophage-mediated inflammatory functions such as the overproduction of cytokines, NO, and PGE2. The CTC was found to be the active fraction in this context.

Protective effect of the methanol extract from Cryptotaenia japonica Hassk. against lipopolysaccharide-induced inflammation in vitro and in vivo.

BACKGROUND: In folk medicine, the aerial part of Crytotaenia japonica Hassk. (CJ), is applied for treatment of the common cold, cough, urinary problems, pneumonia, and skin rashes. In this paper, the in vitro and in vivo anti-inflammatory activity of CJ methanol extract was tested using lipopolysaccharide (LPS)-induced inflammatory models. METHODS: We measured nitric oxide (NO), inducible NO synthase (iNOS), and inflammatory cytokine levels from LPS-stimulated mouse peritoneal macrophages. Also, several cellular signaling molecules which regulate the expressions of these inflammatory markers were examined. Finally, we tested whether oral administration of CJ methanol extract might affect the serum cytokine levels in LPS-injected mice. RESULTS: CJ methanol extract reduced NO release via iNOS protein inhibition. The extract was also shown to decrease the secretions of tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-12. Analysis of signaling molecules showed that CJ inhibited the phosphorylation of STAT1, p38, JNK and ERK1/2 as well as IκBα degradation. Finally, CJ decreased the serum levels of TNF-α and IL-6 in LPS-injected mice. CONCLUSIONS: Our results demonstrated the anti-inflammatory activity of CJ methanol extract and its possible underlying mechanisms that involve modulation of IκBα, MAPK, and STAT1 activities.

Effect of Chrysanthemi borealis flos on atopic dermatitis induced by 1-chloro 2,4-dinitrobenzene in NC/Nga mouse.

The flower of Chrysanthemum boreale has traditionally been used for treatment of various inflammatory disease including atopic dermatitis (AD). However, its action on AD is unclear. Therefore, we investigated the effect of CB on AD using NC/Nga mice as an AD model. The effect of CB on 1-Chloro-2,4-dinitrobenzene (DNCB) induced NC/Nga mice was evaluated by examining skin symptom severity, itching behavior, ear thickness, levels of serum Immunoglobulin E (IgE), tumor necrosis factor-α (TNF-α), and interleukin-4 (IL-4), skin histology. The CB significantly reduced the total clinical severity score, itching behavior, ear thickness and the level of serum IgE in AD mouse model. CB not only decreased TNF-α but also IL-4. These results suggest that CB may be a potential therapeutic modality for AD.

Skeletal growth and IGF levels in rats after HT042 treatment.

HT042, a new herbal prescription consisting of Astragalus membranaceus, Phlomis umbrosa and Eleutherococcus senticosus, is used in traditional Korean medicine to stimulate growth in children. This study was conducted to investigate the effects of HT042 on skeletal growth, insulin-like growth factor-1 (IGF-1) and insulin-like growth factor binding protein-3 (IGFBP-3) levels, and oestrogenic activity in female rats. Female Sprague-Dawley rats were divided into control, recombinant human growth hormone (rhGH; 20 µg/kg/day), and HT042 (100 mg/kg/day) groups and treated for 3 weeks. Axial skeletal growth, femur length, and growth plate length were measured every 3 weeks. The serum IGF-1 and IGFBP-3 levels were analysed. Moreover, the oestrogenic activity of the herbal extracts in the immature and ovariectomized rats was tested. The nose-anus, nose-tail, femur and growth-plate lengths were increased significantly in the HT042 group. Both IGF-1 and IGFBP-3 were highly expressed in the hypertrophic zone of the growth plate. The serum IGF-1 levels were increased. Moreover, HT042 had no uterotrophic effects in the rats. Consequently, HT042 promoted longitudinal bone growth by stimulating cell proliferation in the epiphyseal plate and inducing the expression of IGF-1 without an oestrogenic response. HT042 may be helpful in stimulating growth in children with short stature.

The chloroform fraction of Solanum nigrum suppresses nitric oxide and tumor necrosis factor-α in LPS-stimulated mouse peritoneal macrophages through inhibition of p38, JNK and ERK1/2.

Solanum nigrum L., commonly known as black nightshade, is used worldwide for the treatment of skin and mucosal ulcers, liver cirrhosis and edema. We aimed to determine the anti-inflammatory active fraction of S. nigrum by serial extractions. S. nigrum was first extracted with methanol, then fractionated with chloroform and water. The effects of S. nigrum fractions, diosgenin and α-solanine on LPS/interferon-gamma-induced nitric oxide (NO) and inducible NO synthase (iNOS), or LPS-induced tumor necrosis factor-α (TNF-α) and interleukin (IL)-6, in mouse peritoneal macrophages were determined. Western blotting analysis was used to detect LPS-induced phosphorylation of p38, JNK and ERK1/2. The chloroform fraction of S. nigrum was cytotoxic in a time and concentration dependent manner; however, the methanol and water fractions were not. The chloroform fraction reduced NO through inhibition of iNOS synthesis and inhibited TNF-α and IL-6 at the level of protein secretion; the methanol and water fractions showed a weak or no effect. The chloroform fraction also suppressed p38, JNK and ERK1/2. Diosgenin and α-solanine were cytotoxic at a high concentration. In particular, diosgenin was able to inhibit TNF-α and IL-6, but both compounds did not affect LPS-induced iNOS expression. These results indicate that the anti-inflammatory compounds of S. nigrum exist preferentially in the nonpolar fraction, ruling out the possibility that diosgenin and α-solanine are the likely candidates. The inhibition of iNOS, TNF-α and IL-6 by the chloroform fraction may be partly due to the suppression of p38, JNK and ERK1/2. Further study is required to identify the active compounds of S. nigrum.

Inhibitory effects of Chelidonium majus extract on atopic dermatitis-like skin lesions in NC/Nga mice.

AIM OF THE STUDY: Chelidonium majus (CM) has traditionally been used for treatment of various inflammatory diseases including atopic dermatitis (AD). However its action on atopic dermatitis (AD) is unclear. Therefore, we investigated the effect of CM on AD using NC/Nga mice as an AD model. MATERIALS AND METHODS: The effect of CM on 1-chloro-2,4-dinitrobenzene (DNCB) induced NC/Nga mice was evaluated by examining skin symptom severity, itching behavior, ear thickness, levels of serum immunoglobulin E (IgE), tumor necrosis factor-α (TNF-α), and interlukin-4 (IL-4), skin histology. RESULTS: The CM significantly reduced the total clinical severity score, itching behavior, ear thickness and the level of serum IgE in AD mouse model. CM not only decreased TNF-α but also IL-4. CONCLUSION: These results suggest that CM may be a potential therapeutic modality for AD.