[Effect of electroacupuncture at Jiaji (EX-B2) on disease progression in mice with amyotrophic lateral sclerosis based on NLRP3/Caspase-1/ASC signaling pathway].

Authors

Shilin Wang, Mingyue Wang, Yuanzheng Sun, Guanping Liu, Yingying Li, Wenzhao Zhang, Jia Yao

Published in

Zhongguo zhen jiu = Chinese acupuncture & moxibustion. Volume 46. Issue 10. Pages 1677-1684. Oct 12, 2026. Epub Jul 03, 2026.

Abstract

To explore the underlying mechanism of electroacupuncture (EA) at "Jiaji" (EX-B2) on the disease progression through modulating NOD-like receptor family pyrin domain containing 3 (NLRP3)/cysteine-aspartic acid protease 1 (Caspase-1)/apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC) signaling pathway in mice with amyotrophic lateral sclerosis.
Forty-five mice carrying the human superoxide dismutase 1 G93A (hSOD1^G93A) gene were randomly divided into a model group, a Jiaji EA group, and an inhibitor group, 15 mice per group. The other 15 mice without hSOD1^G93A gene carried were collected as a wild group. When the mice were aged 60 days, in the Jiaji EA group, EA was operated at "Jiaji" (EX-B2) of L₁/L₂, L₅/L₆, with continuous wave, a frequency of 2 Hz and an intensity of 1 mA, retained for 20 min, twice a week; in the inhibitor group, the intraperitoneal injection with NLRP3 inhibitor (10 mg/kg) was administered, twice a week. The interventions lasted for 4 weeks in each group. When the mice were aged 120 days, 9 mice in each group were randomly selected for tissue collection from lumbar spinal cord, and the disease progression and limb function were observed for the remaining 6 mice. The neurological function score was employed to assess the disease progression of mice in each group, and the gait experiment was conducted to observe the gait and stride length; HE staining was used to observe the motor neuron morphology in the anterior horn of the lumbar spinal cord, immunohistochemistry was used to detect the expression of ionic calcium-binding adapter molecule 1 (Iba-1) in the anterior horn of the lumbar spinal cord, and Western blot was used to detect the protein expression of NLRP3, Caspase-1, ASC, interleukin (IL)-18 and IL-1β in lumbar spinal cord.
Compared with the wild group, in the model group, the disease was worsened progressively, on days 90 and 120 after birth, the stride length of mice was reduced (P<0.05, P<0.01), and the gait was unstable and dragging on 120 days after birth; the motor neurons in the anterior horn of the spinal cord exhibited obvious cellular edema and rupture, marked vacuolization and nuclear pyknosis, along with severe neuron loss; the expression of Iba-1 increased in the anterior horn of the lumbar spinal cord (P<0.01), colored dark brown and densely aggregated; and the protein expression of NLRP3, Caspase-1, ASC, IL-18, IL-1β in lumbar spinal cord was up-regulated (P<0.01). When compared with the model group, in the inhibitor group and the Jiaji EA group, the onset of paresis and the progression of paralysis were delayed and the survival rates increased (P<0.01); stride length was larger in the mice at the age of 120 d (P<0.01); more clear gait was presented, and the ages in days was significantly delayed for gait dragging; the improvements were exhibited in the degree of edema, vacuolization, and nuclear pyknosis observed in the motor neurons of the anterior horn of the lumbar spinal cord; the expression of Iba-1 was reduced in the anterior horn of the lumbar spinal cord (P<0.01), appearing gray-brown, and scattered clusters in small number; and the protein expression of NLRP3, Caspase-1, ASC, IL-18, and IL-1β in lumbar spinal cord was decreased (P<0.05, P<0.01). The protein expression of NLRP3, Caspase-1 and IL-18 in lumbar spinal cord in the Jiaji EA group was up-regulated in comparison with that in the inhibitor group (P<0.05).
Electroacupuncture at "Jiaji" (EX-B2) can delay the disease progression in mice with amyotrophic lateral sclerosis, which may be related to modulating NLRP3/Caspase-1/ASC signaling pathway and inhibiting the inflammatory response, thereby attenuating the inflammatory injury of lumbar spinal cord.

PMID:
42864293
Bibliographic data and abstract were imported from PubMed on 13 Oct 2026.

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