The present study sought to investigate the anti-inflammation and immunoloregulation effect of 17 Guizhi Fuling capsule ingredients. The anti-inflammatory ingredients on LPS-induced RAW264. 7 cell injury were assessed with ELISA and immunofluorescence. The release of IL-1β, TNF-α, PGE2 were detected with ELISA and the expression of COX-2 was detected with immunofluorescence. The effects of them on promoting splenic lymphocyte proliferation were assessed with MTT and Hoechst 33342 staining method. The results showed that 15 ingredients had obviously anti-inflammatory activity on LPS- induced injury and play the immunoloregulation roles. This study suggested that the 15 ingredients may be the active ingredients on pelvic infection.
Animals ; Anti-Inflammatory Agents ; pharmacology ; Capsules ; pharmacology ; Cyclooxygenase 2 ; immunology ; Drugs, Chinese Herbal ; administration & dosage ; Immunologic Factors ; pharmacology ; Inflammation ; drug therapy ; Interleukin-1beta ; immunology ; Macrophages ; drug effects ; enzymology ; immunology ; Male ; Mice ; Mice, Inbred BALB C ; Spleen ; cytology ; drug effects ; immunology ; Tumor Necrosis Factor-alpha ; immunology

The anti-inflammatory effects of an ethanol extract of Angelica gigas (EAG) were investigated in vitro and in vivo using croton oil-induced inflammation models. Croton oil (20 microgram/mL) up-regulated mRNA expression of cyclooxygenase (COX)-I and COX-II in the macrophage cell line, RAW 264.7, resulting in the release of high concentrations of prostaglandin E2 (PGE2). EAG (1~10 microgram/mL) markedly suppressed croton oil-induced COX-II mRNA expression and PGE2 production. Application of croton oil (5% in acetone) to mouse ears caused severe local erythema, edema and vascular leakage, which were significantly attenuated by oral pre-treatment with EAG (50~500 mg/kg). Croton oil dramatically increased blood levels of interleukin (IL)-6 and PGE2 without affecting tumor-necrosis factor (TNF)-alpha and nitric oxide (NO) levels. EAG pre-treatment remarkably lowered IL-6 and PGE2, but did not alter TNF-alpha or NO concentrations. These results indicate that EAG attenuates inflammatory responses in part by blocking the COX-PGE2 pathway. Therefore, EAG could be a promising candidate for the treatment of inflammatory diseases.
Angelica/*immunology ; Animals ; Cell Line ; Cyclooxygenase 1/genetics/*immunology ; Cyclooxygenase 2/genetics/*immunology ; Dinoprostone/genetics/immunology ; Inflammation/drug therapy/enzymology/*immunology ; Interleukin-6/blood ; Macrophages ; Male ; Mice ; Mice, Inbred ICR ; Nitric Oxide/blood ; Phytotherapy/*methods ; Plant Extracts/*pharmacology/therapeutic use ; Plant Roots/immunology ; RNA, Messenger/chemistry/genetics ; Reverse Transcriptase Polymerase Chain Reaction ; Tumor Necrosis Factor-alpha/blood

OBJECTIVETo discuss the effect of matrine on nitric oxide (NO) and asymmetric methylarginine (ADMA) metabolism pathways in serum and tissues of mice with lipopolysaccharide (LPS) -induced intestine tissue inflammation.

METHODKunming mice were randomly divided into five groups: the normal control group, the LPS group and matrine (80, 40, 20 mg x kg(-1) x d(-1)) groups. The mice were intragastrically administered with drugs for 3 d (distilled water of the same volume for the normal control group and the LPS group). One hour after the last intragastrical administration, normal saline or LPS (1 mg x kg(-1)) were intraperitoneally injected. Twelve hours later, serum and tissues were collected to determine NO and ADMA levels and observe the pathological changes of intestinal tissues. The Western blot method was adopted to detect the protein expressions of arginine methyltransferases 1 (PRMT1) and dimethylarginine dimethylaminohydrolase 2 (DDAH2) in intestinal tissues.

RESULTCompared with the model group, matrine (80, 40, 20 mg x kg(-1) x d(-1)) groups showed lower NO content in serum and tissues, higher ADMA level in serum and increased PRMT1 expression in intestinal tissues, but without effect on DDAH2 expression.

CONCLUSIONMatrine could inhibit LPS-induced intestine tissue inflammation in mice. Its action mechanism is related to the decreased NO content in serum and tissues and increased ADMA level in serum and PRMT1 expression in intestinal tissues.

Alkaloids ; administration & dosage ; Animals ; Arginine ; analogs & derivatives ; blood ; metabolism ; Humans ; Inflammation ; Intestinal Diseases ; drug therapy ; enzymology ; immunology ; metabolism ; Intestines ; drug effects ; enzymology ; immunology ; metabolism ; Lipopolysaccharides ; adverse effects ; Male ; Mice ; Nitric Oxide ; blood ; metabolism ; Protein-Arginine N-Methyltransferases ; genetics ; metabolism ; Quinolizines ; administration & dosage

OBJECTIVETo evaluate the efficacy of boswellic acid against monosodium urate crystal-induced inflammation in mice.

METHODSThe mice were divided into four experimental groups. Group I served as control; mice in group II were injected with monosodium urate crystal; group III consisted of monosodium urate crystal-induced mice who were treated with boswellic acid (30 mg/kg/b.w.); group IV comprised monosodium urate crystal-induced mice who were treated with indomethacin (3 mg/kg/b.w.). Paw volume and levels/activities of lysosomal enzymes, lipid peroxidation, anti-oxidant status and inflammatory mediator TNF-α were determined in control and monosodium urate crystal-induced mice. In addition, the levels of β-glucuronidase and lactate dehydrogenase were also measured in monosodium urate crystal-incubated polymorphonuclear leucocytes (PMNL) in vitro.

RESULTSThe activities of lysosomal enzymes, lipid peroxidation, and tumour necrosis factor-α levels and paw volume were increased significantly in monosodium urate crystal-induced mice, whereas the activities of antioxidant status were in turn decreased. However, these changes were modulated to near normal levels upon boswellic acid administration. In vitro, boswellic acid reduced the level of β-glucuronidase and lactate dehydrogenase in monosodium urate crystal-incubated PMNL in concentration dependent manner when compared with control cells.

CONCLUSIONSThe results obtained in this study further strengthen the anti-inflammatory/antiarthritic effect of boswellic acid, which was already well established by several investigators.

Animals ; Anti-Inflammatory Agents ; therapeutic use ; Antioxidants ; therapeutic use ; Arthritis, Gouty ; chemically induced ; drug therapy ; Female ; Glucuronidase ; metabolism ; Hydrolases ; metabolism ; Indomethacin ; therapeutic use ; Inflammation ; chemically induced ; drug therapy ; L-Lactate Dehydrogenase ; metabolism ; Lipid Peroxidation ; drug effects ; Male ; Mice ; Neutrophils ; enzymology ; immunology ; Triterpenes ; therapeutic use ; Tumor Necrosis Factor-alpha ; blood ; Uric Acid