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Tannic Acid Provides Neuroprotective Effects Against Traumatic Brain Injury Through the PGC-1α/Nrf2/HO-1 Pathway
Mohd Salman1, Heena Tabassum2, Suhel Parvez3
1Department of Medical Elementology and Toxicology, School of Chemical and Life Sciences, Jamia Hamdard, New Delhi, 110062, India.
Abstract:
The present research was conducted to elucidate a possible molecular mechanism related to neuromodulatory effects of tannic acid (TA) supplementation against traumatic brain injury (TBI) in a rodent model. Oxidative damage and neuroinflammation play a critical role in TBI and lead to behavioral alterations and neuronal dysfunction and death. These changes suggest a potential avenue in neurotherapeutic intervention. The aim of the present study was to investigate the neuroprotective effects of TA and potential mechanism of these effects in a controlled cortical impact injury model of TBI in Wistar rats that were treated with TA (50 mg/kg body weight. i.p.) before 30 min and 6 and 18 h after TBI. TBI-induced rats were examined after 24 h for behavioral dysfunction, Nissl stain, lipid peroxidation rate, glutathione level, activities of antioxidant enzymes (catalase, glutathione S-transferase, glutathione peroxidase, and superoxide dismutase), the expression level of 4-hydroxynonenal, pro-inflammatory cytokines such as tumor necrosis factor alpha and interleukin-1 beta, as well as brain edema and immunoreactivity of glial fibrillary acidic protein. Results indicated that TA supplementation significantly modulated above mentioned alterations. Moreover, TA treatment effectively upregulated the protein expression of peroxisome proliferator-activated receptor gamma co-activator 1 alpha (PGC-1α) and nuclear factor-E2-related factor-2 (Nrf2) as well as mitochondrial transcription factor A and heme oxygenase-1 (HO-1) following TBI. Overall, our results suggest that TA effectively ameliorates the behavioral alterations, oxidative damage, mitochondrial impairment, and inflammation against TBI that may be attributed to activation of PGC-1α/Nrf-2/HO-1 signaling pathway.
Insights
Tannic acid (TA) supplementation effectively reduced oxidative damage, inflammation, and behavioral deficits following traumatic brain injury (TBI) in rats. This neuroprotection is linked to the activation of the PGC-1α/Nrf-2/HO-1 signaling pathway.
Area of Science:
- Neuroscience
- Pharmacology
- Biochemistry
Background:
- Traumatic brain injury (TBI) causes oxidative damage and neuroinflammation, leading to neuronal dysfunction and death.
- Current therapeutic strategies for TBI are limited, highlighting the need for novel neuroprotective agents.
- Tannic acid (TA) has shown potential antioxidant and anti-inflammatory properties.
Purpose of the Study:
- To investigate the neuroprotective effects of tannic acid (TA) in a rodent model of traumatic brain injury (TBI).
- To elucidate the molecular mechanisms underlying TA's neuroprotective effects, focusing on oxidative stress, inflammation, and mitochondrial pathways.
- To evaluate TA's impact on behavioral deficits, neuronal damage, and biochemical markers post-TBI.
Main Methods:
- Wistar rats were subjected to controlled cortical impact injury to model TBI.
- Tannic acid (TA) was administered intraperitoneally at 50 mg/kg before TBI and at 6 and 18 hours post-injury.
- Assessment included behavioral tests, Nissl staining, lipid peroxidation, glutathione levels, antioxidant enzyme activities, inflammatory cytokine expression, brain edema, GFAP immunoreactivity, and Western blot analysis for PGC-1α, Nrf2, Tfam, and HO-1.
Main Results:
- TA treatment significantly ameliorated TBI-induced behavioral deficits, neuronal damage, and brain edema.
- TA administration reduced oxidative stress markers, including lipid peroxidation and 4-hydroxynonenal, while increasing glutathione levels and antioxidant enzyme activities.
- TA upregulated the expression of PGC-1α, Nrf2, Tfam, and HO-1, suggesting activation of a key neuroprotective signaling pathway.
Conclusions:
- Tannic acid (TA) demonstrates significant neuroprotective effects against traumatic brain injury (TBI) in a rodent model.
- TA mitigates TBI-induced oxidative damage, neuroinflammation, and mitochondrial dysfunction.
- The neuroprotective mechanism of TA involves the activation of the PGC-1α/Nrf-2/HO-1 signaling pathway.
