Dataset Information

Antioxidant Activity and Neuroprotective Activity of Stilbenoids in Rat Primary Cortex Neurons via the PI3K/Akt Signalling Pathway.

ABSTRACT: Antioxidant activity and neuroprotective activity of three stilbenoids, namely, trans-4-hydroxystilbene (THS), trans-3,5,4'-trihydroxy-stilbene (resveratrol, RES), and trans-3',4',3,5-tetrahydroxy-stilbene (piceatannol, PIC), against ?-amyloid (A?)-induced neurotoxicity in rat primary cortex neurons were evaluated. THS, RES, and PIC significantly scavenged DPPH• and •OH radicals. All three stilbenoids were able to inhibit A? neurotoxicity by decreasing intracellular reactive oxygen species (ROS) via the PI3K/Akt signalling pathway. Specifically, stilbenoids significantly promoted Akt phosphorylation; suppressed Bcl-2/Bax expression; and inhibited caspase-9, caspase-3, and PARP cleavage. Molecular docking between stilbenoids with Akt indicated that stilbenoids could form hydrogen bond interactions with the COOH-terminal region of Akt. Additionally, the neuroprotective activity of stilbenoids correlated with the number and position of hydroxyl groups. The lack of meta-dihydroxyl groups on THS did not affect its neuroprotective activity in comparison with RES, whereas the ortho-dihydroxyl moiety on PIC significantly enhanced neuroprotective activity. These results provide new insights into the correlation between the biological activity and chemical structure of stilbenoids.

SUBMITTER: Wen H

PROVIDER: S-EPMC6225246 | biostudies-literature | 2018 Sep

REPOSITORIES: biostudies-literature

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Antioxidant Activity and Neuroprotective Activity of Stilbenoids in Rat Primary Cortex Neurons via the PI3K/Akt Signalling Pathway.

Wen Haichao H Fu Zheng Z Wei Yangji Y Zhang Xiaoxu X Ma Liyan L Gu Liwei L Li Jingming J

Molecules (Basel, Switzerland) 20180912 9

Antioxidant activity and neuroprotective activity of three stilbenoids, namely, trans-4-hydroxystilbene (THS), trans-3,5,4'-trihydroxy-stilbene (resveratrol, RES), and trans-3',4',3,5-tetrahydroxy-stilbene (piceatannol, PIC), against β-amyloid (Aβ)-induced neurotoxicity in rat primary cortex neurons were evaluated. THS, RES, and PIC significantly scavenged DPPH• and •OH radicals. All three stilbenoids were able to inhibit Aβ neurotoxicity by decreasing intracellular reactive ...[more]

PMID: 30213108

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Project description:Tendon injury repairs are big challenges in sports medicine, and fatty infiltration after tendon injury is very common and hampers tendon injury healing process. Tendon stem cells (TSCs), as precursors of tendon cells, have shown promising effect on injury tendon repair for their tenogenesis and tendon extracellular matrix formation. Adipocytes and lipids accumulation is a landmark event in pathological process of tendon injury, and this may induce tendon rupture in clinical practice. Based on this, it is important to inhibit TSCs adipogenesis and lipids infiltration to restore structure and function of injury tendon. Aspirin, as the representative of non-steroidal anti-inflammatory drugs (NSAIDs), has been widely used in tendon injury for its anti-inflammatory and analgesic actions, but effect of aspirin on TSCs adipogenesis and fatty infiltration is still unclear. Under adipogenesis conditions, TSCs were treated with concentration gradient of aspirin. Oil red O staining was performed to observe changes of lipids accumulation. Next, we used RNA sequencing to compare profile changes of gene expression between induction group and aspirin-treated group. Then, we verified the effect of filtrated signalling on TSCs adipogenesis. At last, we established rat tendon injury model and compared changes of biomechanical properties after aspirin treatment. The results showed that aspirin decreased lipids accumulation in injury tendon and inhibited TSCs adipogenesis. RNA sequencing filtrated PTEN/PI3K/AKT signalling as our target. After adding the signalling activators of VO-Ohpic and IGF-1, inhibited adipogenesis of TSCs was reversed. Still, aspirin promoted maximum loading, ultimate stress and breaking elongation of injury tendon. In conclusion, by down-regulating PTEN/PI3K/AKT signalling, aspirin inhibited adipogenesis of TSCs and fatty infiltration in injury tendon, promoted biomechanical properties and decreased rupture risk of injury tendon. All these provided new therapeutic potential and medicine evidence of aspirin in treating tendon injury and tendinopathy.

Dataset Information

Antioxidant Activity and Neuroprotective Activity of Stilbenoids in Rat Primary Cortex Neurons via the PI3K/Akt Signalling Pathway.

Publications

Antioxidant Activity and Neuroprotective Activity of Stilbenoids in Rat Primary Cortex Neurons via the PI3K/Akt Signalling Pathway.

Similar Datasets

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