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

To examine the effect of biflorin, a component of Syzygium aromaticum, on memory deficit, we introduced a scopolamine-induced cognitive deficit mouse model. A single administration of biflorin increased latency time in the passive avoidance task, ameliorated alternation behavior in the Y-maze, and increased exploration time in the Morris water maze task, indicating the improvement of cognitive behaviors against cholinergic dysfunction. The biflorin-induced reverse of latency in the scopolamine-treated group was attenuated by MK-801, an NMDA receptor antagonist. Biflorin also enhanced cognitive function in a naïve mouse model. To understand the mechanism of biflorin for memory amelioration, we performed Western blot. Biflorin increased the activation of protein kinase C-ζ and its downstream signaling molecules in the hippocampus. These results suggest that biflorin ameliorates drug-induced memory impairment by modulation of protein kinase C-ζ signaling in mice, implying that biflorin could function as a possible therapeutic agent for the treatment of cognitive problems.
Animals ; Blotting, Western ; Cognition ; Cognition Disorders ; Dizocilpine Maleate ; Hippocampus ; Memory Disorders ; Memory* ; Mice* ; N-Methylaspartate ; Protein Kinases ; Syzygium ; Water

Whereas a somatic pain notifies tissue damage, a neuropathic pain presents disorder of the nerve itself. The causes of neuropathic pains are trauma, infection, chronic irritation by adjacent tissue and so on. The iatrogenic trauma or infection also causes traumatic neuropathy, which may exert a bad influence on doctor-patient relationship. Some of related dental treatments are implantation (directly or indirectly through heating), root canal treatment, teeth extraction, block anesthesia, mandibular surgery. If inappropriate management is performed after nerve trauma, there will be many chances to develop chronic neuropathy for the patient. It is important that the sign of nerve trauma have to be caught by the practitioner as soon as possible and treated properly.
Anesthesia ; Dental Pulp Cavity ; Humans ; Neuralgia ; Nociceptive Pain ; Tooth

Purpose: The isocitrate dehydrogenase (IDH) family plays an essential role in metabolism and energy production. The relative expression levels of IDH isoforms (IDH1, IDH2, and IDH3) have prognostic significance in several malignancies, including breast carcinoma. However, the IDH isozyme expression levels in different cancer stages and types have not been determined in breast carcinoma tissues. Methods: We analyzed the messenger RNA (mRNA) and protein levels of IDH (IDH1, IDH2, and IDH3A) and α-ketoglutarate (α-KG) in 59 breast carcinoma tissues. Results: The mRNA level of IDH2 was significantly increased at stages 2 and 3 in triple-negative and (ER-/PR-/HER+) breast cancers. However, the elevated α-KG level was only observed in stages 2 and 3, with no differences in the various breast carcinoma types. Western blotting analysis showed that IDH2 protein expression increased in the patient tissues and cell lines. An in vitro study showed IDH2 downregulation in the triple-negative breast cancer cell line MDA-MB-231 that inhibited cell proliferation and migration and induced cell cycle arrest in the G0/G1 phase. Conclusion These findings suggest that different from IDH1 and IDH3, IDH2 is more highly expressed in stages 2 and 3 breast cancer tissues, especially in triple-negative breast cancer. IDH2 potentially serves as a target to detect unknown mechanisms in breast cancer.

Anti-inflammatory effects of Houttuynia cordata supercritical extract (HSE) were investigated in a carrageenan-air pouch model. HSE (200 mg/kg, oral) suppressed exudation and albumin leakage, as well as inflammatory cell infiltration. Dexamethasone (2 mg/kg, i.p.) only decreased exudation and cell infiltration, while indomethacin (2 mg/kg, i.p.) reduced exudate volume and albumin content. HSE lowered tumor-necrosis factor (TNF)-alpha and nitric oxide (NO), as well as prostaglandin E2 (PGE2). Dexamethasone only reduced TNF-alpha and NO, while indomethacin decreased TNF-alpha and PGE2. The suppressive activity of HSE on NO and PGE2 production was confirmed in RAW 264.7. These results demonstrate that HSE exerts anti-inflammatory effects by inhibiting both TNF-alpha-NO and cyclooxygenase II-PGE2 pathways.
Analysis of Variance ; Animals ; Anti-Inflammatory Agents/*pharmacology ; Carrageenan ; Cell Line, Tumor ; Dexamethasone/pharmacology ; Dinoprostone/metabolism ; Drugs, Chinese Herbal/*pharmacology ; Immunoenzyme Techniques ; Indomethacin/pharmacology ; Male ; Mice ; Mice, Inbred ICR ; Nitric Oxide/metabolism ; Signal Transduction/*drug effects ; Therapeutic Irrigation ; Tumor Necrosis Factor-alpha/metabolism