Ceftriaxone attenuates glutamate-mediated neuro-inflammation and restores BDNF in MPTP model of Parkinson’s disease in rats
Open accessAbstract
The present study is designed to investigate the role of glutamate transporter in neuroprotection of ceftriaxone against MPTP induced PD animal model. Young male Wistar rats were subjected to intra-nigral administration of MPTP for the induction of Parkinson's disease. Glutamate modulators like ceftriaxone (CFX), Memantine (MEM) and Dihydrokainate (DHK) were administered to MPTP-lesioned rats. Different behavioral alterations were assessed in between the study period. Animals were sacrificed immediately after behavioral session, and different biochemical parameters were measured. Intranigral administration of MPTP showed significant impairment of motor behavior and marked increase in inflammatory mediators and oxidative stress parameters in rats. In addition, MPTP also produced significant decrease in brain-derived neurotrophic factor (BDNF) in striatum of rats. However, chronic administration of ceftriaxone (200mg/kg) has shown significant improvement in motor behavioral deficits and oxidative damage. In addition, Ceftriaxone also attenuated the marked increase of NFκB, TNF-α and IL-1β in MPTP treated rats thus, conferring its neuro-inflammatory property. Further, Ceftriaxone significantly restored the decreased activity of BDNF in striatum of MPTP treated rats. Moreover, pre-treatment of memantine (20mg/kg) with sub-therapeutic dose of ceftriaxone (100mg/kg) potentiated the protective effect of ceftriaxone. Furthermore, intra-nigral injection of DHK (200 nmol) with lower dose of ceftriaxone (100mg/kg) reversed the protective effect of ceftriaxone in MPTP treated rats. The present study concluded that ceftriaxone produce beneficial effect against MPTP induced PD like symptoms rats through glutamatergic pathways.
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Ceftriaxone exhibits a neuroprotective effect in addition to its antibacterial effect in PD.
“it exhibits a neuroprotective effect in addition to its antibacterial effect in PD [15, 20]”
From Neuroprotective Effect of Ceftriaxone on MPTP‐Induced Parkinson’s Disease Mouse Model by Regulating Inflammation and Intestinal Microbiota (2021) · cites this paper as [15]
Ceftriaxone exerts a neuroprotective effect in various neurodegenerative diseases, such as AD, PD, ALS, and HD.
“Subsequent studies have proved that ceftriaxone exerts a neuroprotective effect in various neurodegenerative diseases, such as AD [14], PD [15], amyotrophic lateral sclerosis (ALS) [16], and Huntington's disease (HD) [17].”
From Neuroprotective Effect of Ceftriaxone on MPTP‐Induced Parkinson’s Disease Mouse Model by Regulating Inflammation and Intestinal Microbiota (2021) · cites this paper as [15]
The finding that ceftriaxone restored BDNF and GDNF is consistent with the results of Kaur and Prakash.
“a finding that is consistent with the results of Kaur and Prakash [15]”
From Neuroprotective Effect of Ceftriaxone on MPTP‐Induced Parkinson’s Disease Mouse Model by Regulating Inflammation and Intestinal Microbiota (2021) · cites this paper as [15]
CTX prevents oxidative damage in MPTP-treated rats.
“Similarly, CTX-mediated increase in the main antioxidant modulators glutathione, superoxide dismutase (SOD) and catalase was found to prevent the oxidative damage observed in rats treated with MPTP [233,234].”
From The Interplay between Gut Microbiota and Parkinson’s Disease: Implications on Diagnosis and Treatment (2022) · cites this paper as [233]
CTX reduces TLR-4, MyD88, IL-1β, TNF-α and NF-κB in the brain.
“Further studies proved the ability of CTX to reduce the levels of the main pro-inflammatory mediators TLR-4, MyD88 (myeloid differentiation primary response 88), IL-1β, TNF-α and NF-κB in the brain, TLR-4, MyD88, and NF-κB in the colon and IL-1β, TNF-α and IL-6 in the serum [232,233,234].”
From The Interplay between Gut Microbiota and Parkinson’s Disease: Implications on Diagnosis and Treatment (2022) · cites this paper as [233]
CTX reduces TLR-4, MyD88, and NF-κB in the colon.
“Further studies proved the ability of CTX to reduce the levels of the main pro-inflammatory mediators TLR-4, MyD88 (myeloid differentiation primary response 88), IL-1β, TNF-α and NF-κB in the brain, TLR-4, MyD88, and NF-κB in the colon and IL-1β, TNF-α and IL-6 in the serum [232,233,234].”
From The Interplay between Gut Microbiota and Parkinson’s Disease: Implications on Diagnosis and Treatment (2022) · cites this paper as [233]
CTX reduces IL-1β, TNF-α and IL-6 in the serum.
“Further studies proved the ability of CTX to reduce the levels of the main pro-inflammatory mediators TLR-4, MyD88 (myeloid differentiation primary response 88), IL-1β, TNF-α and NF-κB in the brain, TLR-4, MyD88, and NF-κB in the colon and IL-1β, TNF-α and IL-6 in the serum [232,233,234].”
From The Interplay between Gut Microbiota and Parkinson’s Disease: Implications on Diagnosis and Treatment (2022) · cites this paper as [233]
CTX increases glutathione, SOD and catalase in MPTP-treated rats.
“Similarly, CTX-mediated increase in the main antioxidant modulators glutathione, superoxide dismutase (SOD) and catalase was found to prevent the oxidative damage observed in rats treated with MPTP [233,234].”
From The Interplay between Gut Microbiota and Parkinson’s Disease: Implications on Diagnosis and Treatment (2022) · cites this paper as [233]
CTX reduces glutamatergic hyperactivity in rat PD models.
“At the neuronal level, pre- or post- treatment with CTX prevented the loss of TH-positive neurons, reduced glutamatergic hyperactivity, and promoted neurogenesis at the level of SN and hippocampal dentate gyrus in different rat models of the disease [233,237,238,239,240,241,242].”
From The Interplay between Gut Microbiota and Parkinson’s Disease: Implications on Diagnosis and Treatment (2022) · cites this paper as [233]
CTX administration reverts motor impairment in PD models.
“As a consequence, dyskinesia, motor impairment and memory loss were all reverted upon CTX administration [233,234,237,238,239,240,242,243,244], although conflicting evidence still remains about its ability to improve learning outcomes [245].”
From The Interplay between Gut Microbiota and Parkinson’s Disease: Implications on Diagnosis and Treatment (2022) · cites this paper as [233]
CTX promotes neurogenesis at SN and hippocampal dentate gyrus in rat PD models.
“At the neuronal level, pre- or post- treatment with CTX prevented the loss of TH-positive neurons, reduced glutamatergic hyperactivity, and promoted neurogenesis at the level of SN and hippocampal dentate gyrus in different rat models of the disease [233,237,238,239,240,241,242].”
From The Interplay between Gut Microbiota and Parkinson’s Disease: Implications on Diagnosis and Treatment (2022) · cites this paper as [233]
CTX administration reverts dyskinesia in PD models.
“As a consequence, dyskinesia, motor impairment and memory loss were all reverted upon CTX administration [233,234,237,238,239,240,242,243,244], although conflicting evidence still remains about its ability to improve learning outcomes [245].”
From The Interplay between Gut Microbiota and Parkinson’s Disease: Implications on Diagnosis and Treatment (2022) · cites this paper as [233]
CTX administration reverts memory loss in PD models.
“As a consequence, dyskinesia, motor impairment and memory loss were all reverted upon CTX administration [233,234,237,238,239,240,242,243,244], although conflicting evidence still remains about its ability to improve learning outcomes [245].”
From The Interplay between Gut Microbiota and Parkinson’s Disease: Implications on Diagnosis and Treatment (2022) · cites this paper as [233]
CTX prevents loss of TH-positive neurons in rat PD models.
“At the neuronal level, pre- or post- treatment with CTX prevented the loss of TH-positive neurons, reduced glutamatergic hyperactivity, and promoted neurogenesis at the level of SN and hippocampal dentate gyrus in different rat models of the disease [233,237,238,239,240,241,242].”
From The Interplay between Gut Microbiota and Parkinson’s Disease: Implications on Diagnosis and Treatment (2022) · cites this paper as [233]
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- Authors
- Kaur, B., & Prakash, A.
- Affiliations
- Indo Soviet Friendship College of Pharmacy (IN)
- Johns Hopkins University (US)
- Corresponding author
- Prakash, Atish
- ORCID
- Prakash, Atish
- Venue
- Pathophysiology
- Publisher
- Elsevier BV
- Published
- 2017-06
- Volume
- 24
- Issue
- 2
- Pages
- 71-79
- ISSN
- 0928-4680 (ISSN-L)
- OpenAlex
- W2586325222
- Cited by
- 54
- References
- 44
- Citations by year
- 2026: 4 · 2025: 6 · 2024: 8 · 2023: 3 · 2022: 9 · 2021: 6 · 2020: 3 · 2019: 8 · 2018: 3 · 2017: 3 · 2015: 1
- FWCI
- 3.26
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Pathophysiology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
- Keywords
- ceftriaxone, Parkinson's disease, MPTP, neuroinflammation, glutamate excitotoxicity, brain-derived neurotrophic factor, memantine, dihydrokainate, NF-κB, TNF-α, IL-1β, oxidative stress, motor impairment, neuroprotection, striatum, glutamatergic pathways
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