Molecular biology reports · 2025
Neuroprotective effect of Continentalic acid by targeting NF-κB/Bcl-2 and oxidative stress signaling in traumatic brain injury in male BALB/c mice.
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Zafar Sana, Jamil Maryam, Khan Muhammad Ibrar, Khan Ashraf Ullah, Shah Kifayat Ullah, Seo Eun Kyoung, Khan Salman
Аннотация
BACKGROUND: Traumatic brain injury (TBI) is characterized as a heterogeneous neurological disorder, which causes a variety of behavioral and functional impairments. Continentalic acid (CA), a diterpenoid acid obtained from Aralia continentalis, possesses anti-inflammatory, anti-apoptotic, and antioxidant properties.
METHODS: In the current study we investigated the neuroprotective properties of CA in an experimental TBI model. An in vivo, weight-drop model of TBI was developed in male BALB/c mice. Following traumatic insult, CA (1, 10, and 50 mg/kg) was administered intraperitoneally for up to 14 days. To assess the protective effects of CA, we performed behavioral tests, spectroscopy, histopathology, and biochemical analyses.
RESULTS: The results revealed that CA significantly attenuated trauma-evoked neurological functions and improved mechanical as well as periorbital allodynia. CA also restored the structural and molecular composition of traumatized brain tissues. Similarly, CA reversed the histological changes in the cortex region of the traumatized brain sections and improved the neuronal count. CA administration also decreased the level of traumatic microbleeds in the brain. The expression levels of GFAP and Iba1 were significantly reduced by CA. Treatment with CA significantly reduced the expression of TLR-4, NF-κB, and increased the expression of IĸB-α regulatory protein. CA also downregulated the expression of cleaved caspase-3 protein and upregulated the expression of anti-apoptotic Bcl-2 protein and alleviated the DNA damage. CA dramatically improved the levels of GST, GSH, catalase, and SOD while concomitantly reducing NO and LPO levels. The levels of IL-1β and TNF-α were also reduced in the treatment group.
CONCLUSIONS: The results demonstrated that CA (50 mg/kg) exhibited neuroprotective activity in TBI by attenuating inflammation, neuronal apoptosis, and oxidative stress.
METHODS: In the current study we investigated the neuroprotective properties of CA in an experimental TBI model. An in vivo, weight-drop model of TBI was developed in male BALB/c mice. Following traumatic insult, CA (1, 10, and 50 mg/kg) was administered intraperitoneally for up to 14 days. To assess the protective effects of CA, we performed behavioral tests, spectroscopy, histopathology, and biochemical analyses.
RESULTS: The results revealed that CA significantly attenuated trauma-evoked neurological functions and improved mechanical as well as periorbital allodynia. CA also restored the structural and molecular composition of traumatized brain tissues. Similarly, CA reversed the histological changes in the cortex region of the traumatized brain sections and improved the neuronal count. CA administration also decreased the level of traumatic microbleeds in the brain. The expression levels of GFAP and Iba1 were significantly reduced by CA. Treatment with CA significantly reduced the expression of TLR-4, NF-κB, and increased the expression of IĸB-α regulatory protein. CA also downregulated the expression of cleaved caspase-3 protein and upregulated the expression of anti-apoptotic Bcl-2 protein and alleviated the DNA damage. CA dramatically improved the levels of GST, GSH, catalase, and SOD while concomitantly reducing NO and LPO levels. The levels of IL-1β and TNF-α were also reduced in the treatment group.
CONCLUSIONS: The results demonstrated that CA (50 mg/kg) exhibited neuroprotective activity in TBI by attenuating inflammation, neuronal apoptosis, and oxidative stress.