[Mechanism of electroacupuncture in improving obesity with insulin resistance by regulating the balance of Th17 and Treg cells through SIRT1].

OBJECTIVES

To observe the effect of electroacupuncture (EA) on silent information regulator 1 (SIRT1) and the balance of Th17 and Treg in the adipose tissues of obese rats with insulin resistance, and to explore the mechanisms by which EA improves insulin resistance and obesity.

METHODS

Male Wistar rats were randomly divided into 5 groups:normal group, model group, EA group, sham EA group, and combination group, with 8 rats in each group. An insulin resistance obesity model was established using a high-fat diet. Rats in the EA group received EA at "Zhongwan" (CV12), "Guanyuan" (CV4), "Zusanli" (ST36), and "Fenglong" (ST40), with the needles retained for 10 min each time. The sham EA group underwent superficial needling 5 mm beside the acupoints of the EA group, with electrodes clamped but not powered, while the remaining procedures were identical to those in the EA group. The combination group was administered Sirtinol solution via tail vein injection, with the EA intervention identical to that in the EA group. All interventions were conducted 3 times a week (Monday, Wednesday, and Friday) for 8 weeks. Body mass, Lee's index and glucose infusion rate (GIR) were measured before and after the intervention. Intraperitoneal glucose tolerance tests (IPGTT) were conducted in the 6th week of the intervention period to test the blood glucose level. After the intervention, the percentages of Th17 and Treg cells in the adipose tissue were detected by flow cytometry and the Th17/Treg ratio was calculated, while the relative expression levels of SIRT1, acetylated nuclear factor-κB (AC-NF-κB), and interleukin-17 receptor A (IL-17A) proteins in the adipose tissue of rats in each group were analyzed by Western blot.

RESULTS

Compared with the normal group, the model group showed increased body mass and Lee's index (P<0.05), elevated blood glucose level in IPGTT at all time pionts(P<0.05), decreased GIR (P<0.05), increased percentages of Th17 cells (P<0.05) and decreased percentages of Treg cells (P<0.05) in adipose tissue, and increased Th17/Treg ratio (P<0.05), the expression of SIRT1 protein was decreased (P<0.05) while the expression of Ac-NF-κB and IL-17A proteins were increased (P<0.05) in adipose tissue. Compared with the model group, the EA group showed a significant decrease in body mass and Lee's index (P<0.05), significantly reduced blood glucose level in IPGTT at all time points (P<0.05), increased GIR (P<0.05), decreased percentages of Th17 cells (P<0.05) and increased percentages of Treg cells (P<0.05) in adipose tissue, and reduced Th17/Treg ratio (P<0.05), the expression of SIRT1 protein was increased (P<0.05) while the protein expressions of Ac-NF-κB and IL-17A were decreased (P<0.05) in adipose tissue. Compared with the EA group, the combination group exhibited increases in body mass and Lee's index (P<0.05), elevated blood glucose level at 30, 60, and 120 min post-glucose injection in IPGTT (P<0.05), and decreased GIR (P<0.05), the percentage of Th17 cells was increased (P<0.05) and the Th17/Treg ratio was larger (P<0.05) in adipose tissue, and the expression of SIRT1 protein was reduced (P<0.05) while the protein expressions of Ac-NF-κB and IL-17A were increased (P<0.05) in adipose tissue.

CONCLUSIONS

EA can reduce body mass and improve insulin sensitivity in obese rats, and its mechanism may be related to the activation of SIRT1, which regulates the balance of Th17/Treg and inhibits inflammatory responses.