Rosamultin is one of the main active compounds isolated from Potentilla anserina L., which belongs to a triterpene compound. Few studies have examined the effect of rosamultin on oxidative stress and its molecular mechanism. The aim of this present study was to elucidate the protective effect of rosamultin on H₂O₂‐induced oxidative damage and apoptosis in H9c2 cardiomyocytes and its mechanism. The results showed that the pretreatment of rosamultin not only increased cell viability but also reduced the release of LDH and CK. Rosamultin inhibited a H₂O₂‐induced decrease in SOD, CAT, and GSH‐Px activities and an increase in MDA content. Meanwhile, ROS level, intracellular (Ca²⁺) fluorescence intensity, and apoptosis rate in the rosamultin pretreated group were markedly decreased compared with the model group. Rosamultin pretreatment significantly reversed the morphological changes and attenuated H₂O₂‐induced apoptosis. Western blot analysis showed that rosamultin enhanced the expression of Bcl‐2 and pCryAB and downregulated the expression of Bax, Cyt‐c, Caspase‐3, and Caspase‐9 expression. Additionally, rosamultin might activate PI3K/Akt signal pathways and CryAB relative factors. Therefore, we suggest that rosamultin could have the potential for treating H₂O₂‐induced oxidative stress injury through its antioxidant and antiapoptosis effect.

Hypoxia-inducible factor (HIF)-1α plays a critical role in coupling angiogenesis with osteogenesis during bone development and regeneration. Salidroside (SAL) has shown anti-hypoxic effects in vitro and in vivo. However, the possible roles of SAL in the prevention of hypoxia-induced osteoporosis have remained unknown. Two osteoblast cell lines, MG-63 and ROB, were employed to evaluate the effects of SAL on cell viability, apoptosis, differentiation and mineralization in vitro. Rats subjected to ovariectomy-induced bone loss were treated with SAL in vivo. Our results showed that pre-treatment with SAL markedly attenuated the hypoxia-induced reductions in cell viability, apoptosis, differentiation and mineralization. SAL down-regulated HIF-1α expression and inhibited its translocation; however, SAL increased its transcriptional activity and, consequently, up-regulated vascular endothelial growth factor (VEGF). In vivo studies further demonstrated that SAL caused decreases in the mineral, alkaline phosphatase (ALP) and BGP concentrations in the blood of ovariectomized (OVX) rats. Moreover, SAL improved the trabecular bone microarchitecture and increased bone mineral density in the distal femur. Additionally, SAL administration partially ameliorated this hypoxia via the HIF-1α-VEGF signalling pathway. Our results indicate that SAL prevents bone loss by enhancing angiogenesis and osteogenesis and that these effects are associated with the activation of HIF-1α signalling.

Objective: Chitosan (CS) is currently used as a hemostatic agent in emergencies and in military settings. However, its application is limited owing to its poor hydrophilia at neutral pH. Carboxymethyl chitosan (CMCS) is an important, water-soluble derivative of CS. In this study, we prepared CS and CMCS microspheres (CSMs and CMCSMs, respectively) and evaluated their hemostatic effect.Methods: To prepare the microspheres of various sizes, we used the emulsion cross-linking technique. CMCSMs were also loaded with etamsylate (DIC). Clotting time in vitro and in a hepatic injury model was examined to evaluate the hemostatic effect.Results: CMCSMs swelled more and clotted faster than did CSMs. CMCSMs loaded with DIC had no effect on hemostasis.Conclusions: Both increasing material hydrophilicity and expanding the contact area promoted clotting, whereas chemical cross-linking hampered it because of decreased swelling. CMCSMs are promising candidates for the production of effective hemostatic agents. (Disaster Med Public Health Preparedness. 2017;11:660–667)

As a pair of differential isomers, Kaji-ichigoside F1 and Rosamultin are both pentacyclic triterpenoids isolated from the subterranean root of Potentilla anserina L., a plant used in folk medicine in western China as antihypoxia and anti-inflammatory treatments. We demonstrated that Kaji-ichigoside F1 and Rosamultin effectively prevented hypoxia-induced apoptosis in vascular endothelial cells. We established a hypoxia model, using EA.hy926 cells, to further explore the mechanisms. Hypoxia promoted the phosphorylation of AKT, ERK1/2, and NF-κB. In hypoxic cells treated with Kaji-ichigoside F1, p-ERK1/2 and p-NF-κB levels were increased, while the level of p-AKT was decreased. Treatment with Rosamultin promoted phosphorylation of ERK1/2, NF-κB, and AKT in hypoxic cells. Following the addition of LY294002, the levels of p-AKT, p-ERK1/2, and p-NF-κB decreased significantly. Addition of PD98059 resulted in reduced levels of p-ERK1/2 and p-NF-κB, while p-AKT levels were increased. Pharmacodynamic analysis demonstrated that both LY294002 and PD98059 significantly inhibited the positive effects of Kaji-ichigoside F1 on cell viability during hypoxia, consistent with the results of hematoxylin-eosin (H&E) staining, DAPI staining, and flow cytometry. The antihypoxia effects of Rosamultin were remarkably inhibited by LY294002 but promoted by PD98059. In Kaji-ichigoside F1- and Rosamultin-treated cells, Bcl2 expression was significantly upregulated, while expression of Bax and cytochrome C and levels of cleaved caspase-9 and cleaved caspase-3 were reduced. Corresponding to pharmacodynamic analysis, LY294002 inhibited the regulatory effects of Kaji-ichigoside F1 and Rosamultin on the above molecules, while PD98059 inhibited the regulatory effects of Kaji-ichigoside F1 but enhanced the regulatory effects of Rosamultin. In conclusion, Kaji-ichigoside F1 protected vascular endothelial cells against hypoxia-induced apoptosis by activating the ERK1/2 signaling pathway, which positively regulated the NF-κB signaling pathway and negatively regulated the PI3K/AKT signaling pathway. Rosamultin protected vascular endothelial cells against hypoxia-induced apoptosis by activating the PI3K/AKT signaling pathway and positively regulating ERK1/2 and NF-κB signaling pathways.