Electroacupuncture reduces neuroinflammation and neuronal pyroptosis via downregulating Neat1 in rats after stroke.

Researchers investigated how electroacupuncture (EA) might protect the brain after stroke in rats. Stroke causes inflammation and cell death in the brain, leading to lasting damage. This study explored whether EA works by affecting a specific molecule called Neat1 and reducing a harmful type of cell death called pyroptosis.

The research team used rats with induced strokes and treated some with electroacupuncture at specific points. They measured brain damage, swelling, and neurological function. They also examined brain tissue to see how EA affected inflammation, cell death, and the production of new neurons.

The results showed that electroacupuncture significantly reduced brain damage and improved neurological recovery after stroke. EA decreased levels of Neat1, a molecule that promotes inflammation. When researchers artificially increased Neat1 levels, it blocked many of EA's protective effects. The treatment reduced harmful inflammation in the brain by decreasing inflammatory immune cells and increasing helpful anti-inflammatory signals. EA also protected neurons from pyroptosis, a type of inflammatory cell death that worsens stroke damage. Additionally, the treatment promoted the growth of new brain cells, which may aid recovery.

For patients, this research suggests electroacupuncture may help reduce brain inflammation and cell death after stroke, potentially improving recovery. While these are animal studies and human research is needed, the findings support EA as a complementary therapy for stroke rehabilitation. The study identifies specific biological mechanisms through which acupuncture may work, lending scientific support to its clinical use. Patients interested in electroacupuncture for stroke recovery should consult with a licensed acupuncturist experienced in neurological conditions.

This study examined electroacupuncture's neuroprotective mechanisms in a rat cerebral ischemia/reperfusion injury (CIRI) model. Researchers assessed infarct volume, brain edema, and neurological deficits, employing TUNEL staining, immunofluorescence, qRT-PCR, western blotting, ELISA, and electron microscopy to evaluate the NLRC4 inflammasome pathway and neuronal pyroptosis.

EA significantly downregulated lncRNA Neat1 expression and reduced infarct volume. Neat1 overexpression reversed EA's therapeutic benefits, including neurobehavioral recovery, neuroprotection, and MAP2 preservation. EA inhibited NLRC4 inflammasome activation (NLRC4, Caspase-1, gasdermin D), reducing cellular apoptosis and neuronal pyroptosis—effects blocked by Neat1 overexpression. EA suppressed proinflammatory microglial polarization (Iba1+/CD11b+) while promoting neurogenesis (Nestin+/Sox2+). Neat1 overexpression counteracted EA's modulation of pro- and anti-inflammatory cytokines in ischemic striatum.

Clinical implications: EA appears to exert neuroprotection post-stroke through the Neat1/NLRC4 pathway, inhibiting neuroinflammation and pyroptosis. This mechanism provides molecular evidence supporting EA as adjunctive therapy in stroke management, warranting further clinical investigation.