Salvianolic acid B inhibits Aβ fibril formation and disaggregates preformed fibrils and protects against Aβ-induced cytotoxicty

Effects of Salvia miltiorrhiza on CNS Neuronal Injury and Degeneration: A Plausible Complementary Role of Tanshinones and Depsides

“…SalA ameliorates MPP + -induced ROS production, increases the number of viable cells, inhibits apoptotic pathways, prevents caspase-3 activation, and decreases the number of apoptotic cells. In another study [58], SalA was able to activate Nrf2, inducing HO-1 expression and protecting against oxidative stress in RPE [56] cells by activating the Akt/mammalian target of rapamycin signalling. SalA induced Nrf2 phosphorylation through a mechanism dependent on PI3 K/Akt/mTORC1 activation.…”

“…In addition, SMND-309, a derivative of SalB, increased the survival of neurons and promoted angiogenesis by enhancing EPO and EPOR expression, which subsequently increase CD31 expression via the JAK2/STAT3 and VEGF/Flk-1 pathways [9]. Durairajan and coworkers [56] showed that SalB could inhibit fibril aggregation as well as destabilize preformed Aβ fibril in a dose-and time-dependent manner. SalB might interact with the peptide side chain to inactivate fibril aggregation.…”

Pharmacological actions and therapeutic applications of Salvia miltiorrhiza depside salt and its active components

“…MLB was found to inhibit fibril aggregation as well as to destabilize the preformed Aβ fibrils. Moreover, preincubation with MLB significantly reduced the cytotoxic effect of Aβ 1-42 on human neuroblastoma SH-SY5Y cells [81] . Interestingly, MLB was found to alleviate the memory impairments induced by cholinergic dysfunction or Aβ [25][26][27][28][29][30][31][32][33][34][35] peptide owing to its antagonism of GABA A receptors [82] .…”

Treatment Strategies Targeting Amyloid -Protein

“…This assay ushered in a series of mechanistic publications as well as numerous screens for compounds by both academic and pharmaceutical laboratories. Indeed, proteins, peptides, herbs, natural products and a wide range of small molecules of both known and unknown activities have been shown to block Ab fibrillization (see Table 1 and Lorenzo and Yankner 1994;Tomiyama et al 1994;Bronfman et al 1996;Higaki et al 1997;Kihara et al 1999;Reixach et al 2000;Thomas et al 2001;Ono et al 2002Ono et al , 2004Khurana et al 2003;Blanchard et al 2004;Hirohata et al 2005;Fujiwara et al 2006;Kokkoni et al 2006;Durairajan et al 2008;Ryu et al 2008;Wiesehan et al 2008;Hong et al 2009;Rodriguez-Rodriguez et al 2009). The list of agents is clearly very diverse.…”