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Updated: Sep 19, 2025
Early Pathological and Magnetic Resonance Detection of Cerebral Injury Using a Rat Model of Neonatal Hypoxic Ischemic Encephalopathy
Published on: October 28, 2022
Neuroprotective Effect of Salvianolic Acid C in Neonatal Rats Following Hypoxic-ischemic Brain Damage
Chunfang Dai1,2, Xiaohuan Li3, Zhifang Dong3
1Children's Health Section, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, GuangZhou, 510623, China.
Insights
Salvianolic acid C (SAC) protects neonatal rat brains from hypoxic-ischemic brain damage (HIBD). SAC reduces neuronal loss, oxidative stress, inflammation, and improves motor and cognitive functions, suggesting it may treat HIBD.
Area of Science:
- Neuroscience
- Pharmacology
- Biochemistry
Background:
- Neonatal hypoxia-ischemia (HI) causes severe disabilities and mortality in newborns.
- Neuroprotective effects of Salvianolic acid C (SAC) are known, but its impact on neonatal hypoxic-ischemic brain damage (HIBD) remains unclear.
- Understanding the mechanisms of SAC's neuroprotection is crucial for developing HIBD treatments.
Purpose of the Study:
- To investigate the neuroprotective potential of Salvianolic acid C (SAC) against neonatal hypoxic-ischemic brain damage (HIBD) in a rat model.
- To elucidate the underlying mechanisms, including oxidative stress, JNK pathway, and inflammation, involved in SAC's protective effects.
- To evaluate the functional recovery of motor and cognitive deficits induced by HIBD following SAC administration.
Main Methods:
- Administration of Salvianolic acid C (SAC) at 15 mg/kg/day to rats with HIBD.
- Behavioral tests assessing muscle strength, motor function, and spatial memory.
- Histological analysis to quantify neuron loss in hippocampal CA1 and CA3 zones.
- Biochemical assays to measure oxidative stress markers, JNK pathway activation (p-JNK, c-JUN), and inflammatory cytokines (TNF-α, IL-6, IL-1β).
Main Results:
- SAC administration significantly improved muscle strength, motor function, and spatial memory in HIBD rats.
- SAC treatment markedly reduced neuronal loss in the CA1 and CA3 hippocampal regions.
- SAC enhanced antioxidant production, reduced pro-oxidants, downregulated p-JNK and c-JUN levels, and diminished pro-inflammatory cytokines.
Conclusions:
- Salvianolic acid C (SAC) demonstrates significant neuroprotective effects against neonatal hypoxic-ischemic brain damage (HIBD).
- SAC attenuates neuronal injury by inhibiting oxidative stress, JNK pathway activation, and inflammation.
- SAC improves motor and cognitive deficits in neonatal rats, indicating its potential as a therapeutic agent for neonatal hypoxic-ischemic encephalopathy (HIE).
Abstract:
Neonatal hypoxia-ischemia (HI) is a significant cause of lasting disabilities and death in newborns. Salvianolic acid C (SAC), a phenolic compound extracted from Salvia miltiorrhiza, exhibits neuroprotection. However, it is currently uncertain if SAC displays a neuroprotective impact against neonatal hypoxic-ischemic brain damage (HIBD), and if it does, what mechanism is involved. Here, our study found SAC administration (15 mg/kg/day, i.p.) improved muscle strength, motor function, and spatial memory impairment in rats with HIBD. The amelioration of these behaviors was attributed to a notable suppression of neuron loss by SAC in the CA1 and CA3 hippocampal zones. Moreover, oxidative stress analysis revealed SAC enhanced anti-oxidants production while reducing pro-oxidants production. Western blot assays revealed SAC downregulated the levels of phospho-c-Jun N-terminal kinase (p-JNK) and jun proto-oncogene (c-JUN). ELISA measurements further showed SAC effectively diminished pro-inflammatory factors, including tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β). Collectively, these results suggest SAC exhibits a potential neuroprotective impact by attenuating neuronal injury through inhibiting oxidative stress, JNK pathway activation, and inflammation, thereupon then polishes up motor and cognitive deficits caused by HI in the neonatal rats, indicating SAC may be a promising treatment for neonatal hypoxic-ischemic encephalopathy (HIE).
