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Tibetan golden acupuncture inhibits JNK/caspase-3 signaling pathway to alleviate neuronal apoptosis in cerebral ischemia-reperfusion injury. | LitMetric

AI Article Synopsis

  • Apoptosis due to cerebral ischemia-reperfusion is a major cause of nerve injury, and Tibetan golden acupuncture (GA) is traditionally used to treat this condition in Tibetan medicine.
  • The study involved two experiments to assess the effects of GA on mice subjected to ischemia-reperfusion injury, utilizing behavioral tests and molecular analysis of the JNK signaling pathway.
  • Results indicated that GA significantly improved neurological function and reduced neuronal apoptosis by inhibiting the JNK/caspase-3 pathway, as well as altering the expression of key apoptotic proteins.

Article Abstract

Background: Apoptosis induced by cerebral ischemia-reperfusion is one of the key pathological processes of nerve injury. Tibetan golden acupuncture (GA) is a common treatment for ischemic brain injury in Tibetan. The aim of this study was to explore whether GA prevents cerebral ischemia-reperfusion-induced apoptosis in mice by blocking the JNK/caspase-3 pathway.

Methods: In experiment I, 36 mice were randomly divided into a Sham group, CI/RI group, CI/RI + GA group. Morris water maze tests, TdT-mediated dUTP-biotin nick end labeling (TUNEL) staining and flow cytometry (FCM) were used to evaluate the effect of the GA intervention on CI/RI. In experiment II, 30 mice were randomly divided into a Sham group, CI/RI group, CI/RI + GA group, CI/RI + SP group and CI/RI + SP + EA group. Western blotting was used to detect protein expression of key factors in the JNK signaling pathway in the hippocampus.

Results: After 7 and 14 interventions, behavioral evaluations in CI/RI + GA group was significantly different from those in CI/RI groups (p < 0.01), pathological injury and apoptosis were significantly reduced (p < 0.01). Compared with CI/RI group, the expression of P-JNK/JNK, Cleaved caspase-3/caspase-3, Bax, and Bad proteins in CI/RI + GA group, CI/RI + SP and CI/RI + SP + GA groups were significantly decreased (p < 0.01). The expression of B-cell lymphoma 2 (Bcl-2) was significantly increased (p < 0.01, p < 0.05).

Conclusions: GA can restore neurological dysfunction and inhibit hippocampal neuronal apoptosis in CI/RI mice, at least partially through inhibition of the JNK/Caspase-3 signaling pathway and regulation of apoptosis signals.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11652837PMC
http://dx.doi.org/10.1016/j.heliyon.2024.e40443DOI Listing

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