Review Article

Current Progress of Research on Neurodegenerative Diseases of Salvianolic Acid B

Table 1

Treatment targets, cell lines/animal models, doses, and the possible mechanism of Sal B on neurodegenerative diseases.

Treatment targetsCell lines/animal modelsDosesPossible mechanismReferences

Aβ aggregation and fiber formationPC12 cells10 nmol/LInhibit fibrogenesis of Aβ and damage the formed Aβ fiber; reduce the accumulation of reactive oxygen; inhibit the aggregation and formation of the Aβ1-40 fiber[20]
PC12 cells1-100 μMInhibit Aβ40 fiber formation (IC50: 1.54-5.37 μM); damage the formed Aβ40 fiber (IC50: 5.00-5.19 μM); reduce the accumulation of reactive oxygen induced by Aβ25-35 aggregation[21]
SH-SY5Y-APPsw cells25 μM, 50 μM, 100 μMDecrease the protein expressions of sAPPβ and β-site APP-cleaving enzyme 1; increase the levels of sAPPα and antidisintegrin and metalloprotease 10[22]

Aβ neurotoxicityPC12 cells10 nmol/L, 100 nmol/LReduce toxicity of Aβ40[24]
Injury model on primary rat cortical neuron using 5 μmol/L Aβ400.01 μg/L, 0.10 μg/L, 1.00 μg/LIncrease cell viability; dose-dependently reduce the release rate of LDH and NO; alleviate the toxicity of Aβ40 on the cortical neuron[25]

Tau protein hyperphosphorylationSH-SY5Y cells after incubation with 50 nmol/L OA for 36 h0.072 μg/mL, 0.72 μg/mLIncrease cell activity; reduce the proportion of apoptosis[28]
SH-SY5Y-APPsw cells50 μM, 100 μMIncrease phosphorylation at Ser9 of GSK-3β[22]

Anti-inflammatory and antioxidant effectsRats were intraventricularly injected with Aβ25-3510 mg/kgDecrease the number of microglia (OX-42 positive) and astrocytes (GFAP positive); decrease the mRNA expression of iNOS and COX-2[33]
Mice model of traumatic brain injury25 mg/kgReduce expressions of proinflammatory cytokines TNF-α and IL-1β; increase the expression of anti-inflammatory factors IL-10 and TGF-β1[34]
C57BL/6J mice was exposed to 500 nM Aβ50-400 μMAlleviated intraneuronal glutathione (GSH) and lipid oxidation[35]
Microglia-neuron coculture system50 μM for anti-inflammatoryeffect; 0.5, 5, and 50 μM for antioxidant effectDecrease the production of NO, TNF-α, and IL-1β; decrease the mRNA expressions of iNOS, TNF-α, and IL-1β; dose-dependently reduce the amount of production of ROS in microglia cells; inhibit the activation of transcription factor NF-κB in microglia[36]

ApoptosisPC12 cells treated with Aβ25-3510 nmol/L, 100 nmol/L, 1 μmol/LReduce the proportion of apoptosis[20, 41]
SH-SY5Y cells exposed to MPP+ (500 μΜ)50 μM, 100 μMStabilization of mitochondrial membrane potential; decrease of apoptotic cell number and ROS production; inhibit the release of Cyt c and the activation of caspase-3; reduce bax expression to the normal level; reduce the ratio of bax/bcl-2[43]
PD models of SH-SY5Y exposed to 6-OHDA (100 μM) for 12 h0.1 μM, 1 μM, 10 μMDose-dependently reduce the activity of caspase-3; inhibit the increase in bax and the decrease of bcl-2; increase the proportion of bcl-2/bax[44]

Mitochondrial dysfunctionSH-SY5Y cells exposed to 6-OHDA0.1-10 MAttenuate the decrease of mitochondrial membrane potential and increase of intracellular Ca2+ in a concentration-dependent manner[44]
Primary neurons of C57BL/6J mice exposed to Aβ50-400 μMSuppress excess mitochondrial superoxide generation; protect mitochondrial bioenergetics against Aβ toxicity by preserving mitochondrial membrane potential and ATP production; rescue enzymatic activities of cytochrome c oxidase and F1FO ATP synthase; mitigate axonal mitochondrial fragmentation and increased dynamin-like protein 1 phosphorylation at Ser 616[35]

NeurogenesisNSCs derived from the cortex of fetal mice20 μg/mL, 40 μg/mLPromote the proliferation of NSCs; increase the number of NSCs and cultured neurospheres; promote NSCs to differentiate into neurons[53]
Neural stem/precursor cells (NSPCs)20 μMIncrease the survival rate of NSCs; maintain the self-renewal ability of NSCs by upregulating the mRNA expression of Nestin and Notch-1[54]
Rats with middle cerebral artery occlusion1 mg/kg, 10 mg/kgIncrease the number of SVZ cells[55]
Bone marrow-derived neural stem cells (BM-NSCs)5 mg/mL, 20 mg/mL, 40 mg/mLPromote nestin-positive BM-NSCs to mainly differentiate into NF-M-positive neurons and NG2-positive oligodendrocytes; few of them differentiated into GFAP-positive astrocytes[56]