1. Lobetyolin has a protective role in gastric mucosa injury,and the mechanism may be relate to the increase in level of 6-K-PGF1αand the inhibition the excretion of gastric acid and EGF.
2. Lobetyolin, lobetyol, and methyl linoleate inhibit the gene expression of MUC5AC mucin induced by PMA, however lobetyolin did not affect PMA-induced MUC5AC mucin production.
1. Neohesperidin is a natural new nutrition sweetener, widely existing in plants of dry citrus peel, is particularly suitable for consumption by diabetic patients.
2. Neohesperidin exhibits antioxidant activity (IC50=22.31ug/mL) in the 1,1-diphenyl -2-picryldydrazyl (DPPH) radical-scavenging assay; neohesperidin (50mg/kg) significantly inhibits 55.0% of HCl/ethanol-induced gastric lesions, and increases the mucus content, it may be useful for the treatment and/or protection of gastritis.  3. Neohesperidin can attenuate cerebral ischemia-reperfusion injury via the inhibition of neuronal and oxidative stress through the regulation of the apoptotic pathway and activating the Akt/Nrf2/HO-1 pathway.
4. Neohesperidin and hesperidin have potent anti-inflammatory effects in various inflammatory models, they significantly aggravate gastric damage caused by indomethacin administration as evidenced by increased ulcer index and histopathological changes of stomach.
5. Neohesperidin, Albiflorin, and Aloeemodin have a potent inhibitory effect on Aβ1-40 and Aβ1-42 aggregation, and have neuroprotective effect on primary hippocampal cells against β-Amyloid induced toxicity.
1. Arbutin has whitening, anti- age effects and UVB/ UVC filter by inhibiting tyrosinase and thus preventing the formation of melanin.
2. Normal skin microflora may increase the skin lightening effect of arbutin due to the antioxidant action of hydroquinone.
3. Arbutin has mutagenicity in mammalian cells after activation by human intestinal bacteria.
4. Arbutin has gastroprotective activities.
5. Arbutin is an anti-oxidant and a depigmenting agent, also has anti-inflammatory effect, it may be useful for treating the inflammatory and deleterious effects of BV2 microglial cells activation in response to LPS stimulation.
1. Rutin exerts anti-inflammatory effects in UVB-irradiated mouse skin by inhibiting expression of COX-2 and iNOS, which is attributable to its suppression of p38 MAP kinase and JNK signaling responsible for AP-1 activation.
2. Rutin may protect against spatial memory impairment induced by trimethyltin.
3. Rutin has protective effects on liver injury induced by biliary obstruction in rats, the effect is associated with antioxidative and anti-inflammatory effects as well as the downregulation of NF-κB and TGF-β/Smad signaling, probably via interference of ERK activation and/or enhancement of Nrf2, HO-1, and AMPK activity.
4. Rutin and quercetin have only weak and short-term anticonvulsant potential, they seem to be safe for patients with epilepsy.
5. Rutin(200 mg/kg) has gastroprotective effect through an anti-lipoperoxidant effect, and also by enhancement of the anti-oxidant enzymatic (GSH-Px) activity.
6. Rutin attenuates ischemic neural apoptosis by reducing the expression of p53, preventing morphological changes and increasing endogenous antioxidant enzymatic activities, thus, rutin treatment may represent a novel approach in lowering the risk or improving the function of ischemia–reperfusion brain injury-related disorders.
1. Dehydroabietic acid (DHAA), a major poison to fishes in pulp and paper mill effluents, has toxicological and physiological effects, 20 μg l−1 is close to the “minimum effective concentration” of DHAA to rainbow trout.
2. Dehydroabietic acid derivatives have been reported to display antisecretory and antipepsin effect in animal models, have gastroprotective activity in the HCl/EtOH-induced gastric lesions in mice as well as for cytotoxicity in human lung fibroblasts (MRC-5) and human epithelial gastric (AGS) cells.
3. Dehydroabietic acid derivatives have antiulcer activity.
4. Dehydroabietic acid can reverse several cell responses stimulated by TNF-α, including the activation of FOXO1 and the TGF-β1/Smad3 signaling pathway, suggests that it could be useful in improving the diabetic wound healing.