Anti-inflammatory effects of violaxanthin isolated from microalga Chlorella ellipsoidea in RAW 264.7 macrophages

Violaxanthin is a major carotenoid of microalgae Chlorella ellipsoidea and is also found in dark-green leafy vegetables, such as spinach. In this study, the anti-inflammatory effect of violaxanthin isolated from C. ellipsoidea was examined using lipopolysaccharide (LPS)-stimulated RAW 264.7 mouse macrophage cells. In addition, the anti-inflammatory activity and mechanism of action of purified violaxanthin was assessed using various assays, such as quantitative real-time polymerase chain reaction (PCR), Western blotting, and electrophoretic-mobility shift assay (EMSA). The results of this combined analysis revealed that violaxanthin significantly inhibited nitric oxide (NO) and the prostaglandin E? (PGE?). Interestingly, violaxanthin effectively inhibited LPS-mediated nuclear factor-κB (NF-κB) p65 subunit translocation into the nucleus, suggesting that the violaxanthin anti-inflammatory activity may be based on inhibition of the NF-κB pathways. In conclusion, violaxanthin of C. ellipsoidea holds promise for use as a potential anti-inflammatory agent for either therapeutic or functional adjuvant purposes.     

Anti-inflammatory potential of Phaseolus calcaratus Roxburgh, a oriental medicine, on LPS-stimulated RAW 264.7 macrophages

Objectives The seed of Phaseolus calcaratus Roxburgh (PHCR) has traditionally been used as a herbal medicine, considered to have anti‐inflammatory potential. Here we examined the ability of PHCR seed extract to inhibit inflammatory responses of macrophages to bacterial toxin and the mechanism involved. Methods In the present study, we prepared four fractions from an ethanol extract of PHCR seed and investigated their effects on the production of nitric oxide and cytokines, and the expression of inducible nitric oxide synthase (iNOS) in lipopolysaccharide (LPS)‐stimulated RAW 264.7 macrophage cells. Key findings The fractions inhibited LPS‐induced nitric oxide production and cyclooxygenase‐2 (COX‐2) expression in the cells. The ethyl acetate fraction at 100 µg/ml almost completely suppressed NO production, iNOS and COX‐2 expression, and TNF‐α and IL‐6 secretion in cells stimulated with LPS. The fraction also inhibited phosphorylation of extracellular signal‐regulated kinase (ERK) and p38 in LPS‐stimulated cells with the attendant suppression of IκBα nuclear translocation and nuclear factor (NF)‐κB activation. Furthermore, PHCR seed extracts contained a large number of phenolic compounds having antioxidant potentials against 1,1‐diphenyl‐2‐picrylhydrazyl (DPPH) radicals and hydroxyl radicals. We identified catechin‐7‐O‐β‐d ‐glucopyranoside as one of the active compounds responsible for the biological activity of PHCR seed extract. Conclusions These results suggest for the first time that ethanol extracts from PHCR seed have anti‐inflammatory potential on LPS‐stimulated macrophages through the down‐regulation of ERK/p38‐ and NF‐κB‐mediated signalling pathways.     

Anti-inflammatory effects of dehydrogeijerin in LPS-stimulated murine macrophages

In this study, we investigated whether Heracleum (H) moellendorffii Hance-derived dehydrogeijerin and geijerin could be used to suppress lipopolysaccharide (LPS)-induced inflammatory responses in murine macrophage cell lines, Raw 264.7 cells. Dehydrogeijerin reduced nitric oxide (NO) and inducible nitric oxide synthase (iNOS) production from LPS-stimulated Raw 264.7 cells, but on the other hand, geijerin did not reduce NO production. Dehydrogeijerin, unlike geijerin, has a double bond at C2′–C3′ with an oxo function at C1′. Pre-treatment of Raw 264.7 cells with dehydrogeijerin reduced the production of cyclooxigenase-2 (COX-2) and pro-inflammatory cytokines. These inhibitory effects were associated with decreases in the phosphorylation of mitogen-activated protein (MAP) kinases. Our results indicate that dehydrogeijerin significantly inhibits the inflammatory activity of activated macrophages, suggesting that dehydrogeijerin could be a potential candidate for the treatment of inflammatory disease.     

Anti-inflammatory constituents from the root of Litsea cubeba in LPS-induced RAW 264.7 macrophages

Context Litsea cubeba (Lour.) Pers. (Lauraceae) has long been used as a folk remedy in Traditional Chinese Medicine (TCM) for the treatment of rheumatic diseases. Previous studies from our laboratory indicated that L. cubeba extract showed anti-arthritic activity in rats.

Objective To study L. cubeba chemically and biologically and to find the potential constituents responsible for its anti-arthritic effect.

Materials and methods The compounds were isolated from the root of L. cubeba by column chromatography which eluted with PE:EtOAc gradient system, and the structures were elucidated by detailed spectroscopic data analysis; the anti-inflammatory activity of the isolated compounds was evaluated by lipopolysaccharide (LPS)-induced RAW 264.7 cells and the TNF-α and NO level were measured by ELISA (commercial kit); The iNOS and COX-2 mRNA expression were measured by RT-PCR and the phosphorylation of IκBα, IKKβ, P38 and Akt were determined by western blots.

Results A novel 9-fluorenone, 1-ethoxy-3,7-dihydroxy-4,6-dimethoxy-9-fluorenone (1), together with 4 known compounds, namely pinoresinol (2), syringaresinol (3), 9,9′-O-di-(E)-feruloyl-meso-5,5′-dimethoxysecoisolariciresinol (4) and lyoniresinol (5) were isolated from the root of L. cubeba for the first time. The IC₅₀ for NO inhibition on compounds 1 and 4 were 56.1?±?1.2 and 32.8?±?2.3?μM, respectively. The IC₅₀ for TNF-α inhibition were 28.2?±?0.9 and 15.0?±?1.0?μM, respectively. Both 1 and 4 suppress mRNA expression of iNOS, COX-2 and protein phosphorylation of IκBα, IKKβ in LPS-induced RAW 264.7 cells.

Discussion and conclusion Compounds 1 and 4 isolated from L. cubeba exhibited potent anti-inflammatory activity through the NF-κB signal pathway.     

Anti-inflammatory effect of ethyl acetate extract of Sedum aizoon L. in LPS-stimulated RAW 264.7 macrophages and its HPLC fingerprint

Sedum aizoon L. (SA) has been widely used for treatment of various hemorrhages, insomnia, pain and trauma; however, its anti-inflammatory activity is unknown. In this study, wefirstly investigated the anti-inflammatory activity of SA extracts by petroleum ether (PE), ethyl acetate (EtOAc), and H₂O in LPS-stimulated RAW 264.7 cells. Results showed that the EtOAc extract rich in phenolics and flavonoids significantly inhibited LPS-induced NO, TNF-α, and IL-6 production in RAW 264.7 cells (P<0.01), suggesting that this extract possessed potent anti-inflammatoryactivity. The phytochemical profile of the effective extract was subsequently analyzed by HPLC fingerprint with 11 standards. The results indicated that gallic acid, protocatechuic acid, p-hydroxybenzoic acid, ethyl gallate, iriflophene, 5,7-dihydroxy chromone, quercitrin, quercetin, luteolin, kaempferol, and isorhamnetin were present in this extract, which might contribute to its anti-inflammatory activity. Thus, the EtOAc extract of SA showed anti-inflammatory activity and could be used as a potential natural anti-inflammatory agent.     

Anti-inflammatory effects of Juncus effusus extract (JEE) on LPS-stimulated RAW 264.7 cells and edema models

Context: Juncus effusus L. var. decipiens BUCHEN. f. leschenaultii GAY has been used in traditional medicine for the treatment of anxiety and insomnia.

Objective: The objective of this study was to evaluate the effects of ethanol extract from the pith of Juncus effusus (JEE) on anti-inflammatory activities in RAW 264.7 cells.

Materials and methods: The production of inflammatory mediators and the underlying mechanisms using 3.1, 6.3, and 12.5?μg/mL concentrations of JEE were investigated. In addition, the topical anti-inflammatory effects of JEE (0.5, 1, and 2?mg/mL) on 12-O-tetradecanoylphorobol-13 acetate (TPA)-induced ear edema and oral administration of JEE (50, 100, and 200?mg/kg) on carrageenan-induced paw-edema were studied in mice.

Results: JEE reduced the release of nitric oxide (NO, IC₅₀ value?=?1.98?μg/mL), prostaglandin E₂ (IC₅₀ value?=?5.5?μg/mL), and pro-inflammatory cytokines, IL-1β (IC₅₀ value?=?4.74?μg/mL) and IL-6 (IC₅₀ value?=?20.48?μg/mL). JEE also suppressed the protein expression of inducible NO synthase and cyclooxygenase-2 in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells. Mechanism studies showed attenuation of LPS-induced activation of NF-κB by JEE via abrogation of IκBα degradation and a subsequent decrease in nuclear p65 level. Phosphorylation of all three MAP kinases (ERK, JNK, and p38) in LPS-stimulated RAW 264.7 cells was also suppressed in a dose-dependent manner. In acute inflammation models of mice, topical application (1 and 2?mg) and oral administration (50, 100, and 200?mg/kg) of JEE ameliorated TPA-induced ear edema and carrageenan-induced paw edema, respectively, in dose-dependent manners.

Discussion and conclusion: These results indicate that JEE exhibited anti-inflammatory activities by suppressing the production of inflammatory mediators in LPS-stimulated RAW 264.7 cells and by attenuating edema in mice.     

Inhibitory effects of ivermectin on nitric oxide and prostaglandin E2 production in LPS-stimulated RAW 264.7 macrophages

We have previously shown that ivermectin inhibits LPS-induced production of inflammatory cytokines. In the present study, we investigated the effect of ivermectin on lipopolysaccharide (LPS)-induced nitric oxide (NO) and prostaglandin E₂ (PGE₂) production in RAW 264.7 macrophages. Ivermectin inhibited LPS-induced NO and PGE₂ production. Consistent with these observations, the protein and mRNA expression levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) enzymes were inhibited by ivermectin in a concentration-dependent manner. Furthermore, the phosphorylation of p38, ERK1/2, and JNK in LPS-stimulated RAW 264.7 cells was suppressed by ivermectin in a dose-dependent manner. These results suggest that ivermectin suppresses NO and PGE₂ production, as well as iNOS and COX-2 expression, by inhibiting phosphorylation of mitogen-activated protein kinases (MAPK) (p38, ERK1/2, and JNK) in LPS-stimulated RAW 264.7 cells.     

Anti-inflammatory effect of sargachromanol G isolated from Sargassum siliquastrum in RAW 264.7 cells

A study on the anti-inflammatory activity of brown alga Sargassum siliquastrum led to the isolation of sargachromanol G (SG). In this study, the anti-inflammatory effect and the action mechanism of SG have been investigated in murine macrophage cell line RAW 264.7. SG dosedependently inhibited the production of inflammatory markers [nitric oxide (NO), inducible nitric oxide synthase (iNOS), prostaglandin E(2) (PGE(2)), and cyclooxygenase-2 (COX-2)] and pro-inflammatory cytokines [tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6] induced by LPS treatment. To further elucidate the mechanism of this inhibitory effect of SG, we studied LPS-induced nuclear factor-κB (NF-κB) activation and mitogen-activated protein kinases (MAPKs) phosphorylation. SG inhibited the phosphorylation IκB-α and NF-κB (p65 and p50) and MAPK (ERK1/2, JNK, and p38) in a dose dependent manner. These results suggest that the anti-inflammatory activity of SG results from its modulation of pro-inflammatory cytokines and mediators via the suppression of NF-κB activation and MAPK phosphorylation.     

Inflammatory responses in RAW264.7 macrophages caused by mycobacteria isolated from moldy houses

Mycobacterial strains (nonpathogenic Mycobacterium terrae, potentially pathogenic Mycobacterium avium-complex and Mycobacterium scrofulaceum), isolated from a moldy building, were studied with respect to their ability to stimulate macrophages (RAW264.7) to produce inflammatory mediators, and to cause cytotoxicity. Reactive oxygen species (ROS) were measured by chemiluminescence, cytokines (TNF-, IL-6, IL-1, IL-10) immunochemically, nitric oxide (NO) by Griess-method, expression of inducible NO-synthase (iNOS) with Western Blot analysis and cytotoxicity with MTT-test. All the strains induced dose- and time-dependent production of NO, IL-6 and TNF- in macrophages, whereas IL-1 or IL-10 production was not detected. The production of ROS and cytotoxicity was increased with the highest doses. Interestingly, different strains had significant differences in their ability to induce these responses, M. terrae being the most potent and M. avium-complex the weakest one. These results indicate that both non- and potentially pathogenic strains of mycobacteria present in moldy buildings are capable of activating inflammatory mechanisms in macrophages.     

Anti-inflammatory effects of Dendrobium nobile derived phenanthrenes in LPS-stimulated murine macrophages

Archives of Pharmacal Research - Dendrobium nobile belongs to the Orchidaceae family and is one of the medicinal herbs used in traditional Chinese medicine as a therapeutic agent for...     

Anti-inflammatory effect of pomegranate flower in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages

Context: Punica granatum L (Punicaceae) flower is an important diabetes treatment in oriental herbal medicine.

Objective: This study investigates the inflammation effects of pomegranate flower (PFE) ethanol extract in LPS-induced RAW264.7 cells.

Materials and methods: PFE (10, 25, 50, 100?μg/mL) was applied to 1?μg/mL LPS-induced RAW 264.7 macrophages in vitro. Levels of nitric oxide (NO), prostaglandin E₂ (PGE₂) and pro-inflammatory cytokines interleukin (IL)-1β (IL-1β), interleukin (IL)-6 (IL-6) and tumor necrosis factor (TNF-α) in the supernatant fraction were determined using enzyme-linked immunosorbent assay (ELISA). Expression of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS), phosphorylation of mitogen-activated protein kinase (MAPK) subgroups extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and P38, as well as nuclear factor-κB (NF-κB) activation in extracts were detected via Western blot.

Results: 10–100?μg/mL PFE decreased the production of NO (IC₅₀ value?=?31.8?μg/mL), PGE₂ (IC₅₀ value?=?54.5?μg/mL), IL-6 (IC₅₀ value?=?48.7?μg/mL), IL-1β (IC₅₀ value?=?71.3?μg/mL) and TNF-α (IC₅₀ value?=?62.5?μg/mL) in LPS-stimulated RAW 264.7 cells significantly. A mechanism-based study showed that phosphorylation of ERK1/2, p38, JNK and translocation of the NF-B p65 subunit into nuclei were inhibited by the PFE treatment.

Discussion and conclusion: These results show that PFE produced potential anti-inflammatory effect through modulating the synthesis of several mediators and cytokines involved in the inflammatory process.     

Immunosuppressive activity on the murine immune responses of glycyrol from Glycyrrhiza uralensis via inhibition of calcineurin activity

Context: Calcineurin (CN), a unique protein phosphatase, plays an important role in immune regulation. Our laboratory has established an effective molecular drug-screening model based on CN activity.

Objective: Our aim is to search for an effective immunosuppressant from Glycyrrhiza uralensis (Leguminosae).

Materials and methods: As guided by CN inhibitory test, an active compound was purified and identified as glycyrol. Immunosuppressive activity of glycyrol in vitro was assayed by T lymphocytes proliferation and mixed lymphocyte reaction (MLR). In addition, delayed-type hypersensitivity reaction (DTH) and skin allograft test in vivo were also carried out. Further, we have investigated the effect of glycyrol on phorbol 12-myristate 13-acetate (PMA)/ionomycin (Io)-stimulated IL-2 expression in Jurkat cells.

Results: The enzymatic assay showed glycyrol (IC₅₀?=?84.6?μM) inhibited calcineurin activity in a dose-dependent manner. Glycyrol, at the non-cytotoxic concentration, significantly inhibited proliferation of murine spleen T lymphocytes induced by Concanavalin A (Con A) and mixed lymphocyte reaction (MLR) in vitro. In addition, mice treated with glycyrol had shown the dose-dependent decrease in delayed type hypersensitivity (DTH) and prolonged the graft survival by 59% compared to the control group (*p?<?0.05). RT-PCR showed glycyrol suppressed IL-2 production in a concentration-dependent manner.

Discussion and conclusion: Our results show the immunosuppressive activity of glycyrol and this activity should be due to its inhibitory effect on CN activity, thereby suppressing IL-2 production and regulating T lymphocytes. Thus, glycyrol could be a candidate for development as a novel immunomodulatory drug.     

Anti-inflammatory effects of eriodictyol in lipopolysaccharidestimulated raw 264.7 murine macrophages

Flavonoids have biological activities including anti-allergic, anti-inflammatory, antimicrobial and anticancer activities shown from in vitro studies. Of these biological activities, the anti-inflammatory capacity of flavonoids has long been emphasized in Chinese medicine. In this study, I investigated that what flavonoid can be applied to the suppression of lipopolysaccharide (LPS)-induced inflammatory responses in macrophages among the four similar structure flavonoids. Eriodictyol was found to reduce nitric oxide (NO) production from LPS-stimulated Raw 264.7 cells in non-cytotoxic concentrations. Moreover, eriodictyol strongly suppressed the phagocytic activity of activated macrophages. Pre-treatment of Raw 264.7 cells with eriodictyol reduced the expression of mRNA and the secretion of pro-inflammatory cytokines. These inhibitory effects were found to be caused by blockage of nuclear factor kappa-light-chainenhancer of activated B cells (NF-κB) activation and phosphorylation of p38 mitogen-activated protein kinase (MAPK), extracellular signal-regulated kinases 1 and 2 (ERK1/2) and c-Jun Nterminal kinase (JNK).     

Anti-inflammatory effect of fucoxanthin derivatives isolated from Sargassum siliquastrum in lipopolysaccharide-stimulated RAW 264.7 macrophage

In this study, the anti-inflammatory effect of fucoxanthin (FX) derivatives, which was isolated from Sargassum siliquastrum were evaluated by examining their inhibitory effects on pro-inflammatory mediators in lipopolysaccharide (LPS)-stimulated murine macrophage RAW 264.7 cells. The FX derivatives were isolated from activity-guided chloroform fraction using inhibition of nitric oxide (NO) production and identified as 9′-cis-(6′R) fucoxnathin (FXA), and 13-cis and 13′-cis-(6′R) fucoxanthin complex (FXB) on the basis of a comparison of NMR spectroscopic data. Both FXA and FXB significantly inhibited the NO production and showed slightly reduce the PGE2 production. However, FXB exhibited cytotoxicity at the whole tested concentration, therefore, the results of FXA was only illustrate for further experiments. FXA induced dose-dependent reduction in the inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2) proteins as well as mRNA expression. In addition, FXA reduced the LPS-stimulated production and mRNA expressions of TNF-α and IL-6 in a dose-dependent manner whereas IL-1β production do not inhibit by addition of FXA. Taken together, these findings indicate that the anti-inflammatory properties of FXA may be due to the inhibition of iNOS/NO pathway which associated with the attenuation of TNF-α and IL-6 formation. Thus FXA may provide a potential therapeutic approach for inflammation related diseases.     

Glycoprotein isolated from Rhus verniciflua Stokes inhibits inflammation-related protein and nitric oxide production in LPS-stimulated RAW 264.7 cells

Rhus verniciflua Stokes (RVS) has traditionally been used for medical purpose, such as healing of inflammatory diseases in South Korea. Glycoprotein (36 kDa) was isolated from RVS fruit, purified and used to evaluate the inhibitory effect on inflammatory-related proteins and nitric oxide (NO) production in lipopolysaccharide (LPS, 200 ng/ml)-stimulated RAW 264.7 (murine macrophage cell line). Our results were showed that RVS glycoprotein has a strong antioxidative activity against lipid peroxyl radicals in cell-free system, and inhibits NO production in LPS-stimulated RAW 264.7 cells. To elucidate the inhibitory effect of RVS glycoprotein on activities of inflammatory-related proteins, we firstly evaluated the amount of intracellular reactive oxygen species (ROS), and expression of intracellular protein kinase C (PKC), nuclear factor (NF)-kappaB, and activator protein-1 (AP-1). The results in the present study showed that RVS glycoprotein (200 microg/ml) inhibits ROS production and PKCalpha translocation, and down-regulates the expression of NF-kappaB and AP-1. Such upstream signals consequently inhibited the levels of inducible NO synthase (iNOS) and cyclooxygenase (COX)-2 expression. Therefore, we speculate that RVS glycoprotein inhibits the inflammatory-related protein and can act as an anti-inflammatory agent.     

Evaluation of anti-inflammatory effect of fucoxanthin isolated from brown algae in lipopolysaccharide-stimulated RAW 264.7 macrophages

In this study, potential anti-inflammatory effect of fucoxanthin isolated from brown algae was assessed via inhibitory effect of nitric oxide (NO) production in lipopolysaccharide (LPS) induced RAW 264.7 macrophage cells. The Myagropsis myagroides was selected for further experiments due to its profound NO inhibitory effect, and was partitioned with different organic solvents. Highest NO inhibitory effect was detected in the chloroform fraction, and the active compound was identified as fucoxanthin, a kind of carotenoid available in brown algae evidenced high correlation with the inhibitory effect of NO production (r² = 0.9511). Though, fucoxanthin significantly inhibited the NO production, it slightly reduced the prostaglandin E₂ (PGE₂) production. The inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2) protein expressions were inhibited by fucoxanthin. Further, RT-PCR analysis indicated that the iNOS and COX-2 mRNA expressions were suppressed by fucoxanthin. Moreover, the release of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6), and the mRNA expression levels of those cytokines were reduced by the addition of fucoxanthin in a dose-dependent manner. Hence, these results suggest that the use of fucoxanthin may be a useful therapeutic approach for the various inflammatory diseases.     

Anti-inflammatory activity of hydroxycinnamic acid derivatives isolated from corn bran in lipopolysaccharide-stimulated Raw 264.7 macrophages

In this study, the effect of the 80% ethanolic extract of corn bran (EECB) on inhibition of nitric oxide (NO) production and inducible nitric oxide synthase (iNOS) expression in lipopolysaccharide (LPS)-stimulated Raw 264.7 cells was investigated. The EECB inhibited LPS-induced NO production and iNOS expression in a dose-dependent manner. Four hydroxycinnamic acid derivatives (HADs), including two free cinnamic acids, p-coumaric acid (CA) and ferulic acid (FA), and their conjugate phenolic amides, p-dicoumaroyl-putrescine (DCP) and diferuloylputrescine (DFP), were found to be present in the EECB by LC–MS analysis, and DFP (378.66 μg/g) was the predominant phenolic compound, followed by DCP (7.83 μg/g) > CA (5.58 μg/g) > FA (1.84 μg/g). The four HADs significantly inhibited NO production and iNOS expression in a dose-dependent manner. Among the four HADs tested, DFP showed the most potent inhibition on NO production and iNOS mRNA and protein expression, followed by DCP > FA ? CA. DFP also exhibited the strongest inhibition on LPS-induced iNOS and NF-κB luciferase activity, which was followed by DCP ? FA (CA) > CA (FA). Thus, these results suggest that phenolic amides in the corn bran may be a potential source of natural anti-inflammatory agents.     

Macrophage immunomodulatory activity of polysaccharides isolated from Glycyrrhiza uralensis Fish

The objective of this study was to evaluate the immunomodulatory effects of the purified glycyrrhiza polysaccharides (GP) on the activity of macrophages. A purified fraction of water-soluble polysaccharides, with estimated molecular weight of 10 kDa, was isolated from Glycyrrhiza uralensis Fish using ion exchange and size exclusion chromatography. The results indicate that GP increased the pinocytic activity, the production of nitric oxide (NO), interleukin-1 (IL-1), IL-6 and IL-12 in a dose-dependent manner. The production of IL-1 was induced by GP at a dose of 10 microg/mL; but, NO, IL-6 and IL-12 was significantly induced at 100 microg/mL. A time-dependent enhancement showed that the production of IL-1, NO and IL-12 were significantly increased within 6 h. Superoxide anion (O(2)(-)) production by macrophages from GP-treated mice was higher than that of cells from untreated mice. Moreover, cells from both untreated and treated mice responded to phorbol 12-myristate 13-acetate (PMA) treatment; however, the O(2)(-) production was higher in the cells from treated mice than that of cells from untreated mice. Our data suggest that the beneficial therapeutic effects of GP may be attributed partly to its ability to modulate macrophage immune functions.