What question did this study set out to answer?

To investigate whether activating adenosine monophosphate-activated protein kinase (AMPK) provides neuroprotection by suppressing NLRP3 inflammasome-mediated neuroinflammation in a rat weight-drop model of traumatic brain injury.

September 17, 2026Animal Models and Experimental MedicineOpen Access

Adenosine monophosphate–activated protein kinase activation is associated with suppression of NLRP3 inflammasome–mediated neuroinflammation in a weight‐drop model of traumatic brain injury in Sprague–Dawley rats

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Authors

TKTriveni KodiManipal Academy of Higher Education SPSravan Kumar PakaManipal Academy of Higher Education KNKrishnadas NandakumarManipal Academy of Higher Education

Discussion

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Implication

Animal study demonstrates that AMPK activators attenuate neuroinflammation and cognitive deficits in brain-injured rats, indicating therapeutic potential via NLRP3 inflammasome suppression.

Key Points

To investigate whether activating adenosine monophosphate-activated protein kinase (AMPK) provides neuroprotection by suppressing NLRP3 inflammasome-mediated neuroinflammation in a rat weight-drop model of traumatic brain injury.
Sprague-Dawley rats received daily intraperitoneal injections of vehicle or AMPK activators (metformin 100 mg/kg, quercetin 15 mg/kg, resveratrol 25 mg/kg, cinnamaldehyde 25 mg/kg, or berberine 50 mg/kg) from day -3 to day 17 relative to TBI.
TBI was induced on day 1 via a 240 g weight dropped from a height of 1.5 m.
Outcomes included cognitive testing (novel object recognition and Morris water maze), oxidative stress markers, histopathology, and Western blot/ELISA quantification of p-AMPK, NF-κB, NLRP3, pro-caspase-1, IL-1β, TNF-α, CD86, and CD206.
TBI caused significant cognitive deficits, oxidative stress, and neuronal loss, accompanied by reduced p-AMPK/AMPK ratios, decreased anti-inflammatory CD206, and elevated levels of NF-κB, CD86, TNF-α, and NLRP3 inflammasome components.
Pretreatment with AMPK activators restored the p-AMPK/AMPK ratio and significantly attenuated oxidative stress and histopathological brain damage.
AMPK activation suppressed NLRP3, pro-caspase-1, and IL-1β expression, shifted microglial polarization toward an anti-inflammatory state, and reversed cognitive impairment.

Cite This Study

Kodi et al. (2026) studied this question.

synapsesocial.com/papers/6ab0af898cceb89a47853308 https://doi.org/10.1002/ame2.70288

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September 17, 2026Animal Models and Experimental MedicineOpen Access

Adenosine monophosphate–activated protein kinase activation is associated with suppression of NLRP3 inflammasome–mediated neuroinflammation in a weight‐drop model of traumatic brain injury in Sprague–Dawley rats

View Full Paper

Ask AI

Bookmark

Authors

TKTriveni KodiManipal Academy of Higher Education SPSravan Kumar PakaManipal Academy of Higher Education KNKrishnadas NandakumarManipal Academy of Higher Education

Discussion

Member takes

Implication

Animal study demonstrates that AMPK activators attenuate neuroinflammation and cognitive deficits in brain-injured rats, indicating therapeutic potential via NLRP3 inflammasome suppression.

Key Points

To investigate whether activating adenosine monophosphate-activated protein kinase (AMPK) provides neuroprotection by suppressing NLRP3 inflammasome-mediated neuroinflammation in a rat weight-drop model of traumatic brain injury.
Sprague-Dawley rats received daily intraperitoneal injections of vehicle or AMPK activators (metformin 100 mg/kg, quercetin 15 mg/kg, resveratrol 25 mg/kg, cinnamaldehyde 25 mg/kg, or berberine 50 mg/kg) from day -3 to day 17 relative to TBI.
TBI was induced on day 1 via a 240 g weight dropped from a height of 1.5 m.
Outcomes included cognitive testing (novel object recognition and Morris water maze), oxidative stress markers, histopathology, and Western blot/ELISA quantification of p-AMPK, NF-κB, NLRP3, pro-caspase-1, IL-1β, TNF-α, CD86, and CD206.
TBI caused significant cognitive deficits, oxidative stress, and neuronal loss, accompanied by reduced p-AMPK/AMPK ratios, decreased anti-inflammatory CD206, and elevated levels of NF-κB, CD86, TNF-α, and NLRP3 inflammasome components.
Pretreatment with AMPK activators restored the p-AMPK/AMPK ratio and significantly attenuated oxidative stress and histopathological brain damage.
AMPK activation suppressed NLRP3, pro-caspase-1, and IL-1β expression, shifted microglial polarization toward an anti-inflammatory state, and reversed cognitive impairment.

Cite This Study

Kodi et al. (2026) studied this question.

synapsesocial.com/papers/6ab0af898cceb89a47853308 https://doi.org/10.1002/ame2.70288

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