Ma Zijian,Ma Yang,Cao Xuefeng,Zhang Yunpeng,Song Tieying
Postoperative neurocognitive impairment (POCD) is a common complication after surgery and anesthesia, especially in elderly patients. Avenanthramide-C (AVC) test is a vascular endothelial cell adhesion molecule inhibitor with strong anti-inflammatory and antioxidant effects. The aim of this study was to investigate the effect and mechanism of AVC on POCD in aged rats to clarify the effect of AVC on POCD in aged rats. The aging rat model was established by continuous 200 mg/kg propofol anesthesia. Repeated propofol anesthesia could severely impair spatial learning ability, memory and cognitive function, and could promote hippocampal apoptosis, oxidative stress injury, neuroinflammation and ferroptosis in aging rats. In addition, AVC not only improved cognitive dysfunction, but also significantly inhibited apoptosis, neuroinflammatory response, ferroptosis and oxidative stress level in the hippocampus of aging rats induced by repeated anesthesia. Further mechanistic studies manifested that the above protective effects of AVC on aging rats induced by repeated propofol anesthesia may be achieved by activating Nrf2/ARE pathway activity. AVC pretreatment has a preventive effect on cognitive dysfunction induced by repeated propofol anesthesia in aging rats, and the preventive effect of AVC may be realized by activating the Nrf2/ARE signaling pathway activity. Our results demonstrate that AVC preconditioning reduces postoperative neuronal loss and neuroinflammation, activates the Nrf2/ARE pathway, reduces oxidative stress injury, and improves POCD in aged rats.
Avenanthramide-C (AVN) is a unique ingredient in oats with various bioactivities, but its low gastrointestinal stability limits its application. The AVN was encapsulated with curdlan (CD), oat (OG), and yeast (YG) β-glucans by alkali-neutralization (AN) in this study. Both CD and YG exhibited more ordered aggregation than OG based on Congo red result, possibly contributing to differences in their interaction with AVN. OG-AVN exhibited a higher binding degree (86.57%) than CD-AVN (71.61%) and YG-AVN (81.44%), indicating that the more AVN was retained, the higher solubility and antioxidant capacity of β-glucans-AVN complexes during in vitro digestion. Lower viscoelasticity of OG-AVN and YG-AVN than CD-AVN suggested that the different glycosidic bonds within linear backbone of OG or branches within the triple helix of YG perhaps weakened the tight entanglement, thus providing sufficient regions for AVN binding. Differences in hydrogen bonding structure among β-glucans contributed to their noncovalent interactions with AVN, supported by FTIR (O–H stretching band shift of β-glucans vs. AN-treated ones), XRD (lower relative crystallinity of AVN than complexes), and ITC (higher binding affinity of OG-AVN than YG-AVN and CD-AVN). AFM results supported the change in linear backbone from long to short, which promoted the AVN loading into OG. The binding regions might be located at the OH-7 of AVN with the H-3 of OG or YG, but not CD-AVN, as evidenced by NMR analyses. It demonstrated that the short chains of OG and the branches of YG potentially interacted more easily with AVN, while OG-AVN achieved even better performance.
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