Background: Cudrania tricuspidataextract 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 CHCl₃fraction (CTC) of a methanol extract ofC. tricuspidataon 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)-1β 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-1β, and IL-6 in the LPS-stimulated RAW 264.7 macrophage cells.Conclusions: Our results show that theC. tricuspidataextract 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.

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. 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-β1), and vascular endothelial growth factor (VEGF) were performed by enzyme-linked immunosorbent assay. 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-β1 levels on day 7 and VEGF on day 14 in the serum of scald inflicted SD rat model. 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.

The root of Angelica dahurica Bentham et Hooker (Umbelliferae) has been used as a traditional medicine for colds, headache, dizziness, toothache, supraorbital pain, nasal congestion, acne, ulcer, carbuncle, and rheumatism in China, Japan, and Korea. Interestingly, it has been used in the treatment of vascular diseases including hypertension. The aim of this study was to provide pharmacological evidence for the anti-hypertensive effect of A. dahurica by investigating the mechanism underlying its vasorelaxant effect. The vasorelaxant effects of a 70 % methanol extract of the A. dahurica root (ADE) on rat thoracic aorta and its underlying mechanisms were assessed. Isolated rat aortic rings were suspended in organ chambers containing 10 ml Krebs-Henseleit (K-H) solution and placed between 2 tungsten stirrups and connected to an isometric force transducer. Changes in tension were recorded via isometric transducers connected to a data acquisition system. ADE causes concentration-dependent relaxation in both endothelium-intact and endothelium-denuded aortic rings precontracted with phenylephrine (PE; 1 μM) or potassium (KCl; 60 mM) in K-H solution. And pre-treatment with ADE (1 mg/ml) inhibited calcium-induced vasocontraction of aortic rings induced by PE or KCl. However, ADE pre-treatment did not affect the contraction induced by PE or caffeine in Ca2+-free K-H solution. These results suggested that the ADE has vasorelaxant effect and the vasorelaxant activity is mediated by endothelium-independent pathway that includes the blockade of extracellular calcium influx through the receptor-operated Ca2+ channel and voltage-dependent calcium channel pathways.

Background: Prunus yedoensisMatsum. is used as traditional medicine—‘Yaeng-Pi’ or ‘Hua-Pi’—in Japan and Korea. However, no studies have examined the pharmacological activities of theP. yedoensisbark. Only the antioxidant and antiviral activities ofP. yedoensisfruit and the anti-hyperglycaemic effect ofP. yedoensisleaf have been investigated. While studying the antihypertensive effects of several medicinal plants, we found that a methanol extract ofP. yedoensisbark (MEPY) had distinct vasorelaxant effects on rat aortic rings.Methods: The aortic rings were removed from Sprague–Dawley rats and suspended in organ chambers containing 10 ml Krebs-Henseleit solution. The aortic rings were placed between 2 tungsten stirrups and connected to an isometric force transducer. Changes in tension were recorded via isometric transducers connected to a data acquisition system.Results: MEPY relaxed the contraction induced by phenylephrine (PE) both in endothelium-intact and endothelium-denuded aortic rings concentration dependently. However, the vasorelaxant effects of MEPY on endothelium-denuded aortic rings were lower than endothelium-intact aortic rings. The vasorelaxant effects of MEPY on endothelium-intact aortic rings were reduced by pre-treatment withl-NAME, methylene blue, or ODQ. However, pre-treatment with indomethacin, atropine, glibenclamide, tetraethylammonium, or 4-aminopyridine had no affection. In addition, MEPY inhibited the contraction induced by extracellular Ca²⁺in endothelium-denuded rat thoracic aorta rings pre-contracted by PE (1 μM) or KCl (60 mM) in Ca²⁺-free solution.Conclusions: Our results suggest that MEPY exerts its vasorelaxant effects via the activation of NO formation by means ofl-Arg and NO-cGMP pathways and via the blockage of extracellular Ca²⁺channels.

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.