Background Phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) is one of the essential signaling pathways for the development and maintenance of neuropathic pain. Objective To investigate the effect of resveratrol (RES) on paclitaxel-induced neuropathic pain in rats and elucidate the underlying molecular mechanisms. Method Male Sprague Dawley rats were randomly divided into seven groups (n=10/group): Group C, Group P, Group R, Group R+P, Group LY + R+P, Group LY (the specific inhibitor of PI3K), Group E (the specific inhibitor of sirtuin 1 [SIRT1]). Paw withdrawal mechanical threshold (PWT) and thermal withdrawal latency (TWL) were recorded. Mitochondrial histomorphology was performed by transmission electron microscope. PI3K, p-Akt, and t-Akt expressions were tested using immunohistochemistry. Western blot was used to detect p-Akt, t-Akt, SIRT1, and PGC1α expressions. The apoptosis in the striatum, spinal dorsal horns (SDH), and dorsal root ganglions (DRG) tissues was assayed by TUNEL. ELISA was used to detect the contents of IL-β, IL-10, malondialdehyde (MDA), and superoxide dismutase (SOD) in striatum, SDH, and DRG tissues. Results Compared to the control group, PWT and TWL in the P and LY +R+P groups were significantly decreased on 8th and 14th day after paclitaxel administration ( P <0.05). The expressions of p-Akt, SIRT1, and PGC1α were decreased in paclitaxel-induced neuropathic rats; however, the expressions of p-Akt, SIRT1, and PGC1α were significantly increased after RES treatment ( P <0.05). Furthermore, the expression of p-Akt was decreased by LY294002 ( P <0.05), and amount of SIRT1 and PGC1α expression was inhibited by EX-527 ( P <0.05). The t-Akt level was not significantly changed in all groups. RES prevented paclitaxel-induced mitochondrial damage by PI3K/Akt. RES improves the pain symptoms of paclitaxel neuralgia rats by increasing the IL-10 and decreasing the expression of IL-1β. RES increases the SOD and reduces the MDA. RES reduces apoptosis by SIRT1/PGC1α signal pathway. Conclusion Our results suggest that RES may inhibit paclitaxel-induced neuropathic pain via PI3K/Akt and SIRT1/PGC1α pathways.

PurposeThe purpose of this study was to evaluate the effects of transcutaneous electrical acupoint stimulation (TEAS) on postoperative autonomic nervous system function and serum biomarkers in the elderly.Patients and methodsA total of 122 American Society of Anesthesiologists class II or III patients with coronary heart disease undergoing spinal surgery were randomly divided into two groups: TEAS (received TEAS at Neiguan [PC6] and Ximen [PC4] for 30 minutes before anesthesia induction until the end of surgery) and control (received electrode plate at the same acupuncture points without any electrical stimulation). Serum was isolated for the measurement of concentration of high-sensitive troponin T (hs-cTnT), CRP, and CK. Heart rate (HR) and heart rate variability (HRV) including: total power (TP), low-frequency (LF) power, high-frequency (HF) power, and LF/HF ratio were used to assess autonomic nervous system function. The primary outcome was to evaluate whether TEAS changed the postoperative serum hs-cTnT. The secondary outcomes were to observe the effects of TEAS on HRV, circulating CK and CRP after surgery.ResultsHs-cTnT, CRP, and CK concentrations were significantly higher on first, third and fifth day after surgery than those before anesthesia induction in both groups. Hs-cTnT concentration was significantly lower on the first and third day after surgery in TEAS group than in control group. Compared with 1 day before surgery, TP, LF, and HF decreased significantly and HR, LF/HF increased significantly on first, third, and fifth day after surgery in control group. Compared with control group, HR was significantly lower on the first, third, and fifth day after surgery, LF/HF decreased and TP, LF, HF were significantly higher on the first day after surgery in TEAS group.ConclusionTEAS at PC6 and PC4 could reduce postoperative serum hs-cTnT concentration and change HRV index to improve autonomic nervous system activity.