@article{10.11648/j.ab.20261403.13,
  author = {Ujong Peter Ujong and Mbang Edet Ibor and Precious Takim Mgbe and Edward Odey Emuru and Runyi Bassey Ben and Vivian Peter-Ujong},
  title = {Kolaviron Attenuates Bifenthrin-INDUCED Cerebellar Neurotoxicity Through Multi-Target Modulation of 
NF-κB/Nrf2/p38 MAPK Signaling},
  journal = {Advances in Biochemistry},
  volume = {14},
  number = {3},
  pages = {79-88},
  doi = {10.11648/j.ab.20261403.13},
  url = {https://doi.org/10.11648/j.ab.20261403.13},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ab.20261403.13},
  abstract = {Bifenthrin is a widely used type I pyrethroid insecticide whose exposure has been associated with neurotoxicity mediated by oxidative stress, inflammation, and apoptotic pathways. However, effective protective strategies against bifenthrin-induced cerebellar injury remain inadequately explored. This study investigated the protective effects of kolaviron against bifenthrin-induced cerebellar toxicity in rats and examined the possible involvement of oxidative, inflammatory, and apoptotic signaling pathways. Forty-eight rats were randomly assigned to six groups (n = 8): control, bifenthrin (1 mg/kg), kolaviron (200 mg/kg), kolaviron pretreatment (200 mg/kg) followed by bifenthrin (1 mg/kg), bifenthrin exposure followed by kolaviron post-treatment (200 mg/kg), and kolaviron co-treatment (200 mg/kg) with bifenthrin (1 mg/kg). Treatments were administered for 28 days. Oxidative stress markers, antioxidant enzymes, inflammatory mediators, apoptotic proteins, and relevant signaling molecules were evaluated alongside histopathological changes in the cerebellum. Bifenthrin exposure significantly decreased superoxide dismutase, catalase, glutathione, glutathione peroxidase, glutathione S-transferase, interleukin-4, and nuclear factor erythroid 2-related factor 2 (Nrf2), while significantly increasing malondialdehyde, tumor necrosis factor-α, interleukin-1β, cyclooxygenase-2, inducible nitric oxide synthase, caspase-3, p38 mitogen-activated protein kinase, and nuclear factor-κB (P < 0.05). Histological examination further revealed Purkinje cell degeneration and loss, vacuolation, and inflammatory cell infiltration. Kolaviron significantly ameliorated these biochemical, inflammatory, apoptotic, and histopathological alterations, with pretreatment producing the most consistent protective effects. conclusively, kolaviron attenuates bifenthrin-induced cerebellar toxicity by restoring redox homeostasis, enhancing Nrf2-associated antioxidant defense, and suppressing inflammatory and apoptotic signaling. Its protective activity may involve modulation of the Nrf 2/p38 MAPK/NF-κB signaling axis, resulting in the preservation of cerebellar architecture. These findings highlight kolaviron as a potential protective agent against bifenthrin-induced neurotoxicity.},
 year = {2026}
}

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TY  - JOUR
T1  - Kolaviron Attenuates Bifenthrin-INDUCED Cerebellar Neurotoxicity Through Multi-Target Modulation of 
NF-κB/Nrf2/p38 MAPK Signaling
AU  - Ujong Peter Ujong
AU  - Mbang Edet Ibor
AU  - Precious Takim Mgbe
AU  - Edward Odey Emuru
AU  - Runyi Bassey Ben
AU  - Vivian Peter-Ujong
Y1  - 2026/09/28
PY  - 2026
N1  - https://doi.org/10.11648/j.ab.20261403.13
DO  - 10.11648/j.ab.20261403.13
T2  - Advances in Biochemistry
JF  - Advances in Biochemistry
JO  - Advances in Biochemistry
SP  - 79
EP  - 88
PB  - Science Publishing Group
SN  - 2329-0862
UR  - https://doi.org/10.11648/j.ab.20261403.13
AB  - Bifenthrin is a widely used type I pyrethroid insecticide whose exposure has been associated with neurotoxicity mediated by oxidative stress, inflammation, and apoptotic pathways. However, effective protective strategies against bifenthrin-induced cerebellar injury remain inadequately explored. This study investigated the protective effects of kolaviron against bifenthrin-induced cerebellar toxicity in rats and examined the possible involvement of oxidative, inflammatory, and apoptotic signaling pathways. Forty-eight rats were randomly assigned to six groups (n = 8): control, bifenthrin (1 mg/kg), kolaviron (200 mg/kg), kolaviron pretreatment (200 mg/kg) followed by bifenthrin (1 mg/kg), bifenthrin exposure followed by kolaviron post-treatment (200 mg/kg), and kolaviron co-treatment (200 mg/kg) with bifenthrin (1 mg/kg). Treatments were administered for 28 days. Oxidative stress markers, antioxidant enzymes, inflammatory mediators, apoptotic proteins, and relevant signaling molecules were evaluated alongside histopathological changes in the cerebellum. Bifenthrin exposure significantly decreased superoxide dismutase, catalase, glutathione, glutathione peroxidase, glutathione S-transferase, interleukin-4, and nuclear factor erythroid 2-related factor 2 (Nrf2), while significantly increasing malondialdehyde, tumor necrosis factor-α, interleukin-1β, cyclooxygenase-2, inducible nitric oxide synthase, caspase-3, p38 mitogen-activated protein kinase, and nuclear factor-κB (P < 0.05). Histological examination further revealed Purkinje cell degeneration and loss, vacuolation, and inflammatory cell infiltration. Kolaviron significantly ameliorated these biochemical, inflammatory, apoptotic, and histopathological alterations, with pretreatment producing the most consistent protective effects. conclusively, kolaviron attenuates bifenthrin-induced cerebellar toxicity by restoring redox homeostasis, enhancing Nrf2-associated antioxidant defense, and suppressing inflammatory and apoptotic signaling. Its protective activity may involve modulation of the Nrf 2/p38 MAPK/NF-κB signaling axis, resulting in the preservation of cerebellar architecture. These findings highlight kolaviron as a potential protective agent against bifenthrin-induced neurotoxicity.
VL  - 14
IS  - 3
ER  - 

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