Emodin Promotes Peripheral Nerve Repair by Modulating Inflammasome Activation Through Autophagy via the EGFR/PI3K/AKT/mTOR Pathway DOI Open Access
Z Long, Yuli Huang, Tao Lin

et al.

Phytotherapy Research, Journal Year: 2025, Volume and Issue: unknown

Published: March 26, 2025

To investigate the potential of emodin in promoting nerve regeneration following PNI by targeting macrophage polarization, NLRP3 inflammasome activation, autophagy, and EGFR/PI3K/Akt/mTOR pathway. A cohort 78 male Sprague-Dawley rats was used to develop models sciatic damage, with an additional 18 sham surgery group. The were randomly assigned eight groups: Sham, Control, + Emodin (20 mg/kg), (80 MCC950 (10 Rapamycin (2 mg/kg) 3-MA (15 NSC 228155 (5 mg/kg). administered intragastrical daily, while inhibitors or agonist via intraperitoneal injection, as per respective dosages schedules. treatment period included assessments functional recovery, such histological staining, immunofluorescence for cellular markers, TEM ultrastructural changes, SFI western blot analysis autophagy inflammatory proteins. IF images showed that enhanced axonal myelin regeneration. Histological revealed reduced muscular atrophy collagen deposition. decreased pro-inflammatory markers (CD68) increasing M2 (CD206), inhibited inflammasome, IL-1β caspase-1. It activated Schwann cells, increased LC3-II levels. Network pharmacology molecular docking identified EGFR PI3K/AKT/mTOR pathway a key target, inhibiting activation. This study reveals promotes early recovery enhancing outcomes, remyelination, reducing muscle atrophy. boosts inhibits polarization. These effects are closely related EGFR/PI3K/AKT/mTOR

Language: Английский

Emodin Promotes Peripheral Nerve Repair by Modulating Inflammasome Activation Through Autophagy via the EGFR/PI3K/AKT/mTOR Pathway DOI Open Access
Z Long, Yuli Huang, Tao Lin

et al.

Phytotherapy Research, Journal Year: 2025, Volume and Issue: unknown

Published: March 26, 2025

To investigate the potential of emodin in promoting nerve regeneration following PNI by targeting macrophage polarization, NLRP3 inflammasome activation, autophagy, and EGFR/PI3K/Akt/mTOR pathway. A cohort 78 male Sprague-Dawley rats was used to develop models sciatic damage, with an additional 18 sham surgery group. The were randomly assigned eight groups: Sham, Control, + Emodin (20 mg/kg), (80 MCC950 (10 Rapamycin (2 mg/kg) 3-MA (15 NSC 228155 (5 mg/kg). administered intragastrical daily, while inhibitors or agonist via intraperitoneal injection, as per respective dosages schedules. treatment period included assessments functional recovery, such histological staining, immunofluorescence for cellular markers, TEM ultrastructural changes, SFI western blot analysis autophagy inflammatory proteins. IF images showed that enhanced axonal myelin regeneration. Histological revealed reduced muscular atrophy collagen deposition. decreased pro-inflammatory markers (CD68) increasing M2 (CD206), inhibited inflammasome, IL-1β caspase-1. It activated Schwann cells, increased LC3-II levels. Network pharmacology molecular docking identified EGFR PI3K/AKT/mTOR pathway a key target, inhibiting activation. This study reveals promotes early recovery enhancing outcomes, remyelination, reducing muscle atrophy. boosts inhibits polarization. These effects are closely related EGFR/PI3K/AKT/mTOR

Language: Английский

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