Production of reactive oxygen species by withaferin A causes loss of type collagen expression and COX-2 expression through the PI3K/Akt,p38, and JNK pathways in rabbit articular chondrocytes

Withaferin A (WFA) is a major chemical constituent of Withania somnifera, also known as Indian ginseng. Many recent reports have provided evidence of its anti-tumor, anti-inflammation, anti-oxidant, and immune modulatory activities. Although the compound appears to have a large number of effects, its defined mechanisms of action have not yet been determined.     

Furocoumarins from Angelica pachycarpa

A novel furocoumarin isolated from unripe fruits of Angelica pachycarpa has been characterized as (+)-tert- O-methylbyakangelicin. (+)-tert-O-Methyloxypeucedanin hydrate, neobyakangelicol, (±)-byakangelicol, (+)-byakangelicin, phellopterin, isoimperatorin, oxypeucedanin, oxypeucedanin hydrate, pangeline and umbelliprenin were also identified along with (±)-byakangelicin monoacetate, which proved to be an artifact.     

Methylated Chalcones from Bidens torta

Four new natural products, all methylated chalcones, including an acetylated glycoside, were isolated from Bidens torta. Their structures were determined by spectroscopic methods as okanin 3,4,3′,4′-tetramethyl ether, okanin 3,4,3′-trimethyl ether 4′-glucoside, okanin 4-methyl ether 4′-glucoside and okanin 4-methyl ether 4′-glucoside monoacetate. Okanin 3,4-dimethyl ether 4′-glucoside was also isolated.     

A flavonol glycoside and A sesquiterpene cellobioside from Trillium tschonoskii

The underground and aerial organs of Trillium tschonoskii afforded two new compounds in addition to dioscin, methyl protodioscin and four 18-norspi     

Linarin monoacetate from Thalictrum aquilegifolium

Linarin monoacetate, a new flavonoid glycoside, has been isolated from Thalictrum aquilegifolium and the position of the acetyl group has been determined by ¹³C NMR spectral data.     

Byakangelicin protects against carbon tetrachloride–induced liver injury and fibrosis in mice

Liver fibrosis is a disease caused by long‐term damage that is related to a number of factors. The current research on the treatment of liver fibrosis mainly focuses on the activation of hepatic stellate cell, in addition to protecting liver cells. byakangelicin has certain anti‐inflammatory ability, but its effect on liver fibrosis is unclear. This study aims to explore whether byakangelicin plays a role in the development of liver fibrosis and to explore its mechanism. We determined that byakangelicin has a certain ability to resist fibrosis and reduce liver cell damage in a model of carbon tetrachloride–induced liver fibrosis in mice. Thereafter, we performed further verification in vitro. The signalling pathways of two important pro‐fibrotic cytokines, transforming growth factor‐β and platelet‐derived growth factor, were studied. Results showed that byakangelicin can inhibit related pathways. According to the hepatoprotective effect of byakangelicin observed in animal experiments, we studied the effect of byakangelicin on 4‐HNE–induced hepatocyte (HepG2) apoptosis and explored its related pathways. The results showed that byakangelicin could attenuate 4‐HNE–induced hepatocyte apoptosis via inhibiting ASK‐1/JNK signalling. In conclusion, byakangelicin could improve carbon tetrachloride–induced liver fibrosis and liver injury by inhibiting hepatic stellate cell proliferation and activation and suppressing hepatocyte apoptosis.     

Repair of Cytokine-induced DNA Damage in Cultured Rat Islets of Langerhans

Treatment of cultured rat pancreatic islets of Langerhans with the combined cytokines interleukin-1β (IL-1β), interferon γ (IFN γ) and tumour necrosis factor α (TNF α) leads to DNA damage including strand breakage. We have investigated the nature of this damage and its repairability. When islets are further incubated for 4?h in fresh medium, the level of cytokine-induced strand breakage remains constant. If the nitric oxide synthase inhibitor N^G-monomethyl-l-arginine (NMMA) is present during cytokine treatment, then strand breakage is prevented. If NMMA is added following, rather than during, the cytokine treatment and islets are incubated for 4?h, further nitric oxide synthesis is prevented and most cytokine-induced strand breaks are no longer seen. To investigate DNA repair following cytokine treatment, cells were transferred to fresh medium and incubated for 4?h in the presence of hydroxyurea (HU) and 1-β-d-arabinosyl cytosine (AraC), as inhibitors of strand rejoining. In the presence of these inhibitors there was an accumulation of strand breaks that would otherwise have been repaired. However, when further nitric oxide synthesis was inhibited by NMMA, significantly less additional strand breakage was seen in the presence of HU and AraC. We interpret this, as indicating that excision repair of previously induced base damage did not contribute significantly to strand breakage. Levels of oxidised purines, as indicated by formamidopyrimidine glycosylase (Fpg) sensitive sites, were not increased in cytokine-treated islets. We conclude that in these primary insulin-secreting cells: (a) the DNA damage induced by an 18?h cytokine treatment is prevented by an inhibitor of nitric oxide synthase, (b) much of the damage is in the form of apparent strand breaks rather than altered bases such as oxidised purines, (c) substantial repair is ongoing during the cytokine treatment and this repair is not inhibited in the presence of nitric oxide.     

泽泻化学成分的研究

从泽泻（Alisma orientalis(Sam)Juzep）块茎中分离出12个化合物,经理化性质和波谱分析,分别鉴定为：β-谷甾醇3-O-硬脂酸酯（β-sistosterol-3-O-stearate,1）,正二十三烷（tricosane,2）,β-俗甾醇（β-sitosterol,5）,硬脂酸（stearic acid,6）1-硬脂酸甘油酯（glyeryl 1-stearate,7）,胡萝卜甙6′-O-硬脂酸酯（daucosterol-6′-O-stearate,8）,泽泻醇B单醋酸酯（alisol B monoacetate,9）,大黄素（emodin,10）,泽泻醇C单醋酸酯（alisol C monoacetate,11）,环氧泽泻烯（alismoxide,12）.化合物1,2,5,6,7和10为首次由该植物中获得,化合物12首次以结晶形式获得,化合物3和4的鉴定仍在进行。