Headspace Solid-Phase Microextraction Analysis of Volatile Components in Peanut Oil.

Peanut oil is favored by consumers due to its rich nutritional value and unique flavor. This study used headspace solid-phase microextraction (HS-SPME) combined with gas chromatography (GC) and gas chromatography-mass spectrometry (GC-MS) to examine the differences in the peanut oil aroma on the basis of variety, roasting temperatures, and pressing components. The results revealed that the optimal conditions for extracting peanut oil were achieved through the use of 50/30 µm DVB/CAR/PDMS fibers at 60 °C for 50 min. The primary compounds present in peanut oil were pyrazines. When peanuts were roasted, the temperature raised from 120 °C to 140 °C and the content of aldehydes in peanut oil increased; however, the content of aldehydes in No. 9 oil at 160 °C decreased. The components of peanut shell oil varied depending on the peanut variety. The most marked difference was observed in terms of the main compound at the two roasting temperatures. This compound was a pyrazine, and the content increased with the roasting temperature in hekei oils. When the roasting temperature was lower, No. 9 oil contained more fatty acid oxidation products such as hexanal, heptanal, and nonanal. When the roasting temperature increased, No. 9 oil contained more furfural and 5-methylfurfural. Heren oil was easier to oxidize and produced nonanal that possessed a fatty aroma.

Phenylpropanoids and lignoids from the whole plant of Vaccinium emarginatum and their cytotoxicity against prostate cancer cells.

One new naturally occurring quinone, 3',4'-dihydroxy-1,2,6-trimethoxy-[1,1'-biphenyl]-4(1H)-one (1), one new diarylpropane, emarginone A (2), and one new neolignan, emarginone B (3), along with eighteen known compounds have been isolated from the chemical investigation of the EtOAc-soluble fraction of the Vaccinium emarginatum whole plant methanolic extract. The new structures were elucidated by combined analysis of spectroscopic analytical methods and comparison with the literature data obtained from known analogues. In addition, the cytotoxicity of compounds 2, 4, and 14-20 against Du145 and PC-3 prostate cancer cell lines using MTT cell proliferation assay was evaluated. Compounds 2 and 19 showed most potent cytotoxicity against Du145 with IC50 values of 7.53 and 6.63 µg/mL, respectively. Furthermore, compounds 2, 17, and 19 also exhibited significant cytotoxicity against PC-3 with IC50 values ranging from 3.44-6.64 µg/mL.

Composition and Insecticidal Activity of Essential Oil of Bacopa caroliniana and Interactive Effects of Individual Compounds on the Activity.

Bacopa caroliniana (BC) is a perennial creeping herb and popular aquarium plant. This plant is easily cultivated; consequently, it has the potential to be a raw material which is readily available for mass production if it contains useful bioactive substances. The information about the functionality of this plant has been very limited. Therefore, the aims of this research were to analyze the composition of the essential oil (EO) of BC and to study its insecticidal effect on rice weevils. Moreover, the interactive effects of active compounds of the EO on this activity were also investigated. A total of 18 volatile compounds was identified, accounting for ca. 94% of the BC-EO in terms of quantity. Of them, α-terpinolene was the largest compound. The impact of individual volatile compounds on the inhibition of acetylcholine esterase and insecticidal activity were determined. α-Terpinolene exhibited the highest activity on these assays. Both additive and synergistic effects existed in terms of the insecticidal activity. Many compounds found in the BC-EO are widely present in other EOs. Thus, the information obtained from this study is useful for EO-related research, applications in selecting EOs or in seeking the best combination of EOs or individual compounds to achieve efficient insecticidal effects.

Identification of ß-Sitosterol as in Vitro Anti-Inflammatory Constituent in Moringa oleifera.

ß-Sitosterol is a well known phytosterol in plants, but owing to its poor solubility in typical media, determining its cellular mechanisms has been proven to be difficult. In this study, we investigated the anti-inflammatory activity of ß-sitosterol (BSS) isolated from Moringa oleifera in two cell lines. Over a dose range of 7.5 to 30 µM, BSS dispersed well in the medium as nanoparticles with diameters of 50 ± 5 nm and suppressed the secretion of inflammatory factors from keratinocytes and macrophages induced by PGN, TNF-α, or LPS, such as TNF-α, IL-1ß, IL-6, IL-8, and ROS, separately. In addition, BSS significantly reduced the expression of NLRP3, a key component of NLRP3 inflammasomes, and inhibited the activation of caspase-1. There was partial inhibition of NF-κB in macrophages. This is the first study to report an increase in the solubility of nearly water-insoluble phytosterols via the formation of nanoparticles and to delineate the formulation's capacity to inhibit the signal transduction pathways of inflammation in macrophages.

Assessment of biochemical and immunomodulatory activity of sulphated polysaccharides from Ulva intestinalis.

The biochemical characteristics and immunomodulatory activity of sulphated polysaccharides isolated from Ulva intestinalis and fractionated using a silica-silica column were investigated. The unfractionated (USP) and fractionated sulphated polysaccharides (FSP4, FSP30, and FSP32) consisted mostly of carbohydrates (4.84-26.55%) and sulphates (2.85-20.42%). Structural analyses showed that USP, FSP4, FSP30 and FSP32 had molecular weights of 300, 80, 110 and 140kDa, respectively. FSP30 exhibited the strongest DPPH radical scavenging activity. Moreover, FSP30 showed stronger immunomodulatory activities than UPS in term of stimulating the production of pro-inflammatory cytokines, including nitric oxide (NO), tumour necrosis factor-α (TNF-α), and interleukin-1ß (IL-1ß), in macrophage J774A.1 cells. USP and FSP30 were not cytotoxic to mouse macrophage at the tested concentrations (6.25-50µg/mL). The results suggested that U. intestinalis polysaccharides could be explored as potential antioxidant and immunomodulatory agents to be used as complementary medicine or functional foods.

Resveratrol inhibits NLRP3 inflammasome activation by preserving mitochondrial integrity and augmenting autophagy.

The NLRP3 inflammasome is a caspase-1-containing multi-protein complex that controls the release of IL-1ß and plays important roles in the development of inflammatory disease. Here, we report that resveratrol, a polyphenolic compound naturally produced by plants, inhibits NLRP3 inflammasome-derived IL-1ß secretion and pyroptosis in macrophages. Resveratrol inhibits the activation step of the NLRP3 inflammasome by suppressing mitochondrial damage. Resveratrol also induces autophagy by activating p38, and macrophages treated with an autophagy inhibitor are resistant to the suppressive effects of resveratrol. In addition, resveratrol administration mitigates glomerular proliferation, glomerular sclerosis, and glomerular inflammation in a mouse model of progressive IgA nephropathy. These findings were associated with decreased renal mononuclear leukocyte infiltration, reduced renal superoxide anion levels, and inhibited renal NLRP3 inflammasome activation. Our data indicate that resveratrol suppresses NLRP3 inflammasome activation by preserving mitochondrial integrity and by augmenting autophagy.

Osthole improves an accelerated focal segmental glomerulosclerosis model in the early stage by activating the Nrf2 antioxidant pathway and subsequently inhibiting NF-κB-mediated COX-2 expression and apoptosis.

Inflammatory reactions and oxidative stress are implicated in the pathogenesis of focal segmental glomerulosclerosis (FSGS), a common chronic kidney disease with relatively poor prognosis and unsatisfactory treatment regimens. Previously, we showed that osthole, a coumarin compound isolated from the seeds of Cnidium monnieri, can inhibit reactive oxygen species generation, NF-κB activation, and cyclooxygenase-2 expression in lipopolysaccharide-activated macrophages. In this study, we further evaluated its renoprotective effect in a mouse model of accelerated FSGS (acFSGS), featuring early development of proteinuria, followed by impaired renal function, glomerular epithelial cell hyperplasia lesions (a sensitive sign that precedes the development of glomerular sclerosis), periglomerular inflammation, and glomerular hyalinosis/sclerosis. The results show that osthole significantly prevented the development of the acFSGS model in the treated group of mice. The mechanisms involved in the renoprotective effects of osthole on the acFSGS model were mainly a result of an activated Nrf2-mediated antioxidant pathway in the early stage (proteinuria and ischemic collapse of the glomeruli) of acFSGS, followed by a decrease in: (1) NF-κB activation and COX-2 expression as well as PGE2 production, (2) podocyte injury, and (3) apoptosis. Our data support that targeting the Nrf2 antioxidant pathway may justify osthole being established as a candidate renoprotective compound for FSGS.

Antimicrobial activity of the essential oil of Glossogyne tenuifolia against selected pathogens.

BACKGROUND: Glossogyne tenuifolia (GT) is a perennial herb widely distributed in the areas from south Asia to Australia. Many biological effects of G. tenuifolia have been reported; however, the information about antimicrobial activity of the essential oil (EO) of the herb remains unavailable. Therefore, the aims of this study were to investigate the antimicrobial activity of the GT-EO in vitro and food systems, the antimicrobial impact (AI) of its individual compounds, and interactive effects of major active compounds (linalool, 4-terpineol, α-terpineol, ρ-cymene) on selected Gram-positive (S. aureus, L. monocytogenes, S. mutans and S. sanguinis) and Gram-negative (E. coli O157:H7, V. parahaemolyticus and S. enterica) pathogens. RESULTS: The minimal microbicidal concentration (MMC) of the GT-EO ranged from 0.75 to 12 mg mL(-1) against the test bacteria in vitro. Except for L. monocytogenes, the GT-EO exhibited more inhibitory effect on the selected Gram positive than against the Gram negative bacteria at the GT-EO concentrations ≤ 12 mg mL(-1) . The interactive effects of major active compounds (linalool, 4-terpineol, α-terpineol, ρ-cymene) are additive instead of synergistic via the checkerboard analysis. The bacteria with a microbial load of ca. 10(2) CFU mL(-1) in the milk tea could be completely inactivated by the GT-EO with the MMC of 1.5 mg mL(-1) . CONCLUSION: ρ-Cymene is the largest component in the GT-EO; however, it is not the compound predominantly affecting the entire antimicrobial activity of the EO. Instead, 4-terpineol is the most influential among the test compounds that contribute to the antimicrobial activity of the GT-EO.

Osthole mitigates progressive IgA nephropathy by inhibiting reactive oxygen species generation and NF-κB/NLRP3 pathway.

Renal reactive oxygen species (ROS) and mononuclear leukocyte infiltration are involved in the progressive stage (exacerbation) of IgA nephropathy (IgAN), which is characterized by glomerular proliferation and renal inflammation. The identification of the mechanism responsible for this critical stage of IgAN and the development of a therapeutic strategy remain a challenge. Osthole is a pure compound isolated from Cnidiummonnieri (L.) Cusson seeds, which are used as a traditional Chinese medicine, and is anti-inflammatory, anti-apoptotic, and anti-fibrotic both in vitro and in vivo. Recently, we showed that osthole acts as an anti-inflammatory agent by reducing nuclear factor-kappa B (NF-κB) activation in and ROS release by activated macrophages. In this study, we examined whether osthole could prevent the progression of IgAN using a progressive IgAN (Prg-IgAN) model in mice. Our results showed that osthole administration resulted in prevention of albuminuria, improved renal function, and blocking of renal progressive lesions, including glomerular proliferation, glomerular sclerosis, and periglomerular mononuclear leukocyte infiltration. These findings were associated with (1) reduced renal superoxide anion levels and increased Nrf2 nuclear translocation, (2) inhibited renal activation of NF-κB and the NLRP3 inflammasome, (3) decreased renal MCP-1 expression and mononuclear leukocyte infiltration, (4) inhibited ROS production and NLRP3 inflammasome activation in cultured, activated macrophages, and (5) inhibited ROS production and MCP-1 protein levels in cultured, activated mesangial cells. The results suggest that osthole exerts its reno-protective effects on the progression of IgAN by inhibiting ROS production and activation of NF-κB and the NLRP3 inflammasome in the kidney. Our data also confirm that ROS generation and activation of NF-κB and the NLRP3 inflammasome are crucial mechanistic events involved in the progression of the renal disorder.

Anti-inflammatory lanostanoids and lactone derivatives from Antrodia camphorata.

Four new lanostanoids, ethyl lucidenate A (1), ethyl lucidenate F (2), 15-O-acetylganolucidate A (3), and 3,11,15,23-tetraoxo-27ξ-lanosta-8,16-dien-26-oic acid (4), and two new lactone derivatives, 5-hydroxy-5-(methoxymethyl)-4-methylfuran-2(5H)-one (5) and 3-(4-methoxy-2-oxo-2H-pyran-6-yl)propanoic acid (6), together with four known compounds, 11α-hydroxy-3,7-dioxolanost-8,24(E)-dien-26- oic acid (7), 3,7,11-trioxo-5α-lanosta-8,24(E)-dien-26-oic acid (8), methyl 3,7,11,12,15,23-hexaoxo-5α-lanost-8-en-26-oate (9), and ethyl 3,7,11,12,15,23-hexaoxo-5α-lanost-8-en-26-oate (10), were characterized from Antrodia camphorata. The structures of these new compounds were determined by analysis of their spectroscopic data, including 1D and 2D NMR experiments. Ten components were evaluated for anti-inflammatory activity by examining their effect on LPS-iNOS-dependent NO production in murine macrophage (RAW 264.7) cells. Among them, compounds 1, 3, 7, 8, 9, and 10 significantly suppressed the NO concentration in LPS-treated RAW 264.7 cells with IC50 values ≤ 10 µM.

Diterpenoids with anti-inflammatory activity from the wood of Cunninghamia konishii.

Two new diterpenoids, konishone (1) and 3b-hydroxy-5,6-dehydrosugiol (2), along with three known diterpenoids--hinokiol (3), sugiol (4), and 12-hydroxy-6,7-secoabieta-8,11,13-triene-6,7-dial (5)--were isolated from the wood of Cunninghamia konishii. Compound 1 is a novel skeleton of the 7,20-dinorabietane-type diterpene. In addition, when RAW264.7 macrophages were treated with different concentrations of compounds 1, 3, and 5 together with LPS, a significant concentration-dependent inhibition of NO production was detected. The IC50 values for inhibition of nitrite production of compounds 1, 3, and 5 were about 9.8 ± 0.7, 7.9 ± 0.9, and 9.3 ± 1.3 µg/mL, respectively. This study presents the potential utilization of compounds 1, 3, and 5, as lead compounds for the development of anti-inflammatory drugs.

Lipopolysaccharide/adenosine triphosphate-mediated signal transduction in the regulation of NLRP3 protein expression and caspase-1-mediated interleukin-1ß secretion.

OBJECTIVE: Reactive oxygen species (ROS) plays a critical role in the regulation of NLRP3 inflammasome activation. However, the ROS-mediated signaling pathways controlling NLRP3 inflammasome activation are not well defined. METHODS: Using lipopolysaccharide (LPS) and adenosine triphosphate (ATP) activated murine macrophages as the testing model, cytokine release and protein expression were quantified by enzyme-linked immunosorbent assay and Western blot, respectively. ROS was scavenged by N-acetyl cysteine; NADPH oxidase, the major source of ROS, was inhibited by diphenyliodonium, apocynin or gp91-phox siRNA transfection; and protein kinase was inhibited by its specific inhibitor. RESULTS: LPS-induced NLRP3 protein expression was regulated through the NADPH oxidase/ROS/NF-κB-dependent, JAK2/PI3-kinase/AKT/NF-κB-dependent, and MAPK-dependent pathways, while ATP-induced caspase-1 activation was regulated through the NADPH oxidase/ROS-dependent pathway. CONCLUSIONS: These results demonstrate that ROS regulates not only the priming stage, but also the activation stage, of NLRP3 inflammasome activation in LPS + ATP-activated macrophages.

Improved purity and immunostimulatory activity of ß-(1→3)(1→6)-glucan from Pleurotus sajor-caju using cell wall-degrading enzymes.

The objective of this work was to improve the purity of ß-(1→3)(1→6)-glucan in the native triple helical structure from the fruiting bodies of Pleurotus sajor-caju for effective biological function using cell wall-degrading enzymes. A crude carbohydrate was extracted with hot water, then treated with crude xylanase and cellulase from Paenibacillus curdlanolyticus B-6. ß-Glucan in the extract was purified to homogeneity with a single and symmetrical peak using 650M DEAE Toyopearl and Sepharose CL-6B column chromatography. The purity of ß-glucan was confirmed by high-performance size-exclusion chromatography. Purified ß-glucan was obtained at a purity of up to 90.2%. The Congo red reaction and atomic force microscopy indicated that the purified ß-glucan exhibited a triple helix conformation. Purified ß-glucan was able to effectively up-regulate the functions of macrophages such as nitric oxide (NO) and tumor necrosis factor (TNF-α) production.

Osthole regulates inflammatory mediator expression through modulating NF-κB, mitogen-activated protein kinases, protein kinase C, and reactive oxygen species.

Osthole, a coumarin compound, has been reported to exhibit various biological activities; however the cellular mechanism of its immune modulating activity has not yet been fully addressed. In this study we isolated osthole from the seeds of Cnidium monnieri and demonstrated that osthole inhibited TNF-α, NO and COX-2 expression in LPS-stimulated macrophages, without reducing the expression of IL-6. Furthermore, the phosphorylation of p38, JNK1/2, PKC-α and PKC-ε induced by LPS was inhibited by osthole; however, the phosphorylation of ERK1/2 and PKC-δ was not reduced by osthole. Osthole also inhibited NF-κB activation and ROS release in LPS-stimulated macrophages. Our current results indicated that osthole is the major anti-inflammatory ingredient of Cnidium monnieri seed ethanol extract.

Structure and functions of gamma-dodecalactone isolated from Antrodia camphorata for NK cell activation.

The preserved fungal species Antrodia camphorata has diverse health-promoting effects and has been popularly used in East Asia as a traditional herb. We isolated a volatile compound from the culture medium of A. camphorata and identified it as gamma-dodecalactone (gamma-DDL). Cytomic screening for immune-modulating activity revealed that gamma-DDL can activate human NK cells to express the early activation marker CD69. Further experiments showed that gamma-DDL not only can induce NK cells to express CD69 but also stimulate NK cells to secrete cytotoxic molecules (FasL and granzyme B) and Th1 cytokines (TNF-alpha and INF-gamma). Measuring the distribution of gamma-DDL in the subcellular compartments of NK cells revealed that gamma-DDL has been converted to 4-hydroxydodecanoic acid (an acyclic isomer of gamma-DDL) in a time-dependent manner in the cytoplasm. Synthetic (R,S)-4-hydroxydodecanoic acid activated NK cells to express CD69 mRNA within 10min, in contrast to gamma-DDL, which activated NK cells to express CD69 within 50min. This faster activation suggests that gamma-DDL has converted to 4-hydroxydodecanoic acid and to stimulate the NK cells to express CD69. Optically pure (R)-(+)-4-hydroxydodecanoic acid and (S)-(-)-4-hydroxydodecanoic acid were obtained via: (1) synthesis of its diastereomeric esters of (R,S)-4-hydroxydodecanoic (R)-(-)-2-phenylpropionate; (2) separation of diastereomers via preparative HPLC, and (3) subsequent hydrolysis of the obtained optical pure ester of (R)-(+)-4-hydroxydodecanoic acid (R)-(-)-2-phenylpropionate and (R)-(-)-4-hydroxydodecanoic acid (R)-(-)-2-phenylpropionate, respectively. Further assays of NK cells activation using each enantiomer showed that only the (R)-(+)-4-hydroxydodecanoic acid can activate NK cells.

Anti-inflammatory bioactivities of honokiol through inhibition of protein kinase C, mitogen-activated protein kinase, and the NF-kappaB pathway to reduce LPS-induced TNFalpha and NO expression.

Much recent research has demonstrated that honokiol, a phenolic compound originally isolated from Magnolia officinalis, has potent anticancer activities; however, the detailed molecular mechanism of its anti-inflammatory activity has not yet been fully addressed. In this study we demonstrated that honokiol inhibited lipopolysaccharide (LPS)-induced tumor necrosis factor-alpha secretion in macrophages, without affecting the activity of the tumor necrosis factor-alpha converting enzyme. At the same time, honokiol not only inhibited nitric oxide expression in LPS-stimulated murine macrophages but also inhibited the LPS-induced phosphorylation of ERK1/2, JNK1/2, and p38. By means of confocal microscope analysis we demonstrated that phosphorylation and membrane translocation of protein kinase C-alpha, as well as NF-kappaB activation, were inhibited by honokiol in LPS-stimulated macrophages. Furthermore, it was found that honokiol neither antagonizes the binding of LPS to cells nor alters the cell surface expression of toll-like receptor 4 and CD14. Our current results have exhaustively described the anti-inflammatory properties of honokiol, which could lead to the possibility of its future pharmaceutical application in the realm of immunomodulation.

Immunostimulatory bioactivity of algal polysaccharides from Chlorella pyrenoidosa activates macrophages via Toll-like receptor 4.

Much research suggests that a dietary supplement of Chlorella pyrenoidosa may be helpful to human health, but the molecular mechanism involved remains unclear. The aim of this research was to investigate the effects of certain hot-water-soluble polysaccharides from Chlorella pyrenoidosa (CWSP) on cytokine production, human leukocyte antigen (HLA) expression, and costimulatory molecule expression in macrophages. We demonstrated that CWSP induced IL-1beta secretion in macrophages via Toll-like receptor 4 (TLR4) mediated protein kinase signaling pathways. In addition, CWSP also stimulated the cell surface expression of HLA-DA, -DB, and -DC, and HLA-DR, -DP, and -DQ as well as the expression of costimulatory family molecules such as CD80 and CD86 in macrophages. Furthermore, we demonstrated that preinjection of C57BL/6J mice with CWSP increased lipopolysaccharide (LPS)-induced tumor necrosis factor-alpha and IL-1beta secretion into serum in vivo. This outcome was consistent with the corresponding outcome for cells treated with CWSP in vitro. Our current results provide support for the possible use of CWSP as a modulation agent of immune responses in humans and certain animal species. Finally, in using GC-MS to analyze the polysaccharides, we found that the major monosaccharides of CWSP were rhamnose (31.8%), glucose (20.42%), galactose (10.28%), mannose (5.23%), and xylose (1.27%). This study is the first to report the molecular mechanism of immune-modulated signal transduction in vitro from the polysaccharides of Chlorella pyrenoidosa.

Heme oxygenase-1 mediates the anti-inflammatory effect of Curcumin within LPS-stimulated human monocytes.

Curcumin, a polyphenolic compound derived from plant, regulates heme oxygenase (HO-1) expression within certain cell types; however, the Curcumin-mediated signal transduction in the regulation of HO-1 expression within human monocytes/macrophages is unclear. Herein, we show that Curcumin dose dependently induced HO-1 expression and HO-1 activity through the activation of PKCalpha, PKCdelta/ERK1/2, p38alpha, and PI3-kinase. In addition, H2O2 release is essential for Curcumin-mediated ERK1/2 and p38 phosphorylation and HO-1 expression. Further, Curcumin inhibited LPS-induced IL-1 and IL-6 secretion and blockage of HO-1 expression/activity by HO-1 siRNA or HO-1 inhibitor, SnPP reversed the inhibitory effects of Curcumin on cytokines secretion. HO-1 over-expression produced the same inhibitory effects of Curcumin on IL-1 secretion. Collectively, our results suggest that Curcumin inhibits cytokines secretion within LPS-stimulated monocytes through a mechanism that involves the action of HO-1.

Cinnamaldehyde inhibits pro-inflammatory cytokines secretion from monocytes/macrophages through suppression of intracellular signaling.

We investigated the in vitro anti-inflammatory effects of Cinnamaldehyde, a cytokine production inhibitor isolated from an essential oil produced from the leaves of Cinnamomum osmophloeum Kaneh, and its mechanism of action. Although Cinnamaldehyde has been reported to have contact sensitizing properties at high concentration (mM), we found that low concentration of Cinnamaldehyde (muM) inhibited the secretion of interleukin-1beta and tumor necrosis factor alpha within lipopolysaccharide (LPS) or lipoteichoic acid (LTA) stimulated murine J774A.1 macrophages. Cinnamaldehyde also suppressed the production of these cytokines from LPS stimulated human blood monocytes derived primary macrophages and human THP-1 monocytes. Furthermore, Cinnamaldehyde also inhibited the production of prointerleukin-1beta within LPS or LTA stimulated human THP-1 monocytes. Reactive oxygen species release from LPS stimulated J774A.1 macrophages was reduced by Cinnamaldehyde. The phosphorylation of extracellular signal-regulated kinase 1/2 and c-Jun N-terminal kinase 1/2 induced by LPS was also inhibited by Cinnamaldehyde; however, Cinnamaldehyde neither antagonize the binding of LPS to the cells nor alter the cell surface expression of toll-like receptor 4 and CD14. In addition, we also noted that Cinnamaldehyde appeared to elicit no cytotoxic effect upon J774A.1 macrophages under our experimental conditions, although Cinnamaldehyde reduced J774A.1 macrophages proliferation as analysed by MTT assay. Our current results have demonstrated the anti-oxidation and anti-inflammatory properties of Cinnamaldehyde that could provide the possibility for Cinnamaldehyde's future pharmaceutical application in the realm of immuno-modulation.

Ganoderma lucidum polysaccharides enhance CD14 endocytosis of LPS and promote TLR4 signal transduction of cytokine expression.

We have previously reported that a well-characterized glycoprotein fraction containing fucose residues in an extract of Ganoderma lucidum polysaccharides (EORP) exerts certain immuno-modulation activity by stimulating the expression of inflammatory cytokines via TLR4. Continuing our studies, we have demonstrated that EORP increases the surface expression of CD14 and TLR4 within murine macrophages J774A.1 cells in vitro, and further promotes LPS binding and uptake by J774A.1 cells in a CD14-dependent fashion. Moreover, we observed the co-localization of internalized LPS with lysosome- and Golgi-apparatus markers within 5 min after J774A.1 cells stimulated with LPS. In addition, EORP pretreatment of J774A.1 cells and human blood-derived primary macrophages, followed by LPS stimulation, results in the super-induction of interleukin-1beta (IL-1) expression. Endocytosis inhibitors: such as cytochalasin D and colchicine effectively block EORP-enhanced LPS internalization by J774A.1 cells; yet they fail to decrease the LPS-induced phosphorylation of certain mitogen-activated protein kinases, and IL-1 mRNA and proIL-1 protein expression, indicating that LPS internalization by J774A.1 cells is not associated with LPS-dependent activation. Our current results could provide a potential EORP-associated protection mechanism for bacteria infection by enhancing IL-1 expression and the clearance of contaminated LPS by macrophages.