Reversal of cisplatin triggered neurotoxicity by Acacia hydaspica ethyl acetate fraction via regulating brain acetylcholinesterase activity, DNA damage, and pro-inflammatory ... View Full Text


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Article Info

DATE

2022-07-05

AUTHORS

Tayyaba Afsar, Suhail Razak, Ali Almajwal

ABSTRACT

BackgroundCisplatin (CisPT) is a chemotherapeutic that outcome in adverse effects including neurotoxicity. We examined the efficacy of hydaspica ethyl acetate extract (AHE) against CisPT-prompted neurotoxicity.MethodsGroup I: Distilled water; Group II: CisPT (12 mg/kg b.w. i.p) on the 13th day of treatment. Group III: received AHE (400 mg/kg b.w) orally for 16 days. Group IV and V received 200 and 400 mg/kg b.w AHE orally for 16 days while CisPT injection on day 13, respectively. Group VI: received Silymarin (100 mg/kg b.w) orally for 16 days and CP (12 mg/kg b.w., i.p.) on day 13. TNF-α, IL6, brain acetylcholinesterase activity (AChE), oxidative trauma markers, genotoxicity, antioxidant enzymes, and morphological alterations in cerebral hemispheres were inspected.ResultsAHE administration before CisPT considerably reduced both tissue TNF-α and IL 6 expressions compared to CisPT treated group in a dose-dependent manner. AHE treatment (400 mg/kg b.w) significantly ameliorated brain AChE activity. Brain tissue MDA, H2O2, and NO content were markedly (p < 0.001) elevated after CisPT inoculation while a noticeable (p < 0.001) diminution was observed in AHE treatment groups. AHE treatment significantly (p < 0.001) improved brain antioxidant defense in a dose-dependent manner. Furthermore, AHE efficiently recused CisPT to induce DNA damage in brain tissue as revealed by ladder assay and DNA fragmentation patterns. Histopathological findings revealed severe neurodegenerations in CisPT treated group, however, AHE treatment noticeably precluded morphological alterations and neuron damages induced by CisPT.ConclusionA. hydaspica AHE extract may be provided as a prospective adjuvant that precludes CisPT-induced neurotoxicity due to its radical scavenging and antioxidant potential. More... »

PAGES

179

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    http://scigraph.springernature.com/pub.10.1186/s12906-022-03657-3

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    39 schema:description BackgroundCisplatin (CisPT) is a chemotherapeutic that outcome in adverse effects including neurotoxicity. We examined the efficacy of hydaspica ethyl acetate extract (AHE) against CisPT-prompted neurotoxicity.MethodsGroup I: Distilled water; Group II: CisPT (12 mg/kg b.w. i.p) on the 13th day of treatment. Group III: received AHE (400 mg/kg b.w) orally for 16 days. Group IV and V received 200 and 400 mg/kg b.w AHE orally for 16 days while CisPT injection on day 13, respectively. Group VI: received Silymarin (100 mg/kg b.w) orally for 16 days and CP (12 mg/kg b.w., i.p.) on day 13. TNF-α, IL6, brain acetylcholinesterase activity (AChE), oxidative trauma markers, genotoxicity, antioxidant enzymes, and morphological alterations in cerebral hemispheres were inspected.ResultsAHE administration before CisPT considerably reduced both tissue TNF-α and IL 6 expressions compared to CisPT treated group in a dose-dependent manner. AHE treatment (400 mg/kg b.w) significantly ameliorated brain AChE activity. Brain tissue MDA, H2O2, and NO content were markedly (p < 0.001) elevated after CisPT inoculation while a noticeable (p < 0.001) diminution was observed in AHE treatment groups. AHE treatment significantly (p < 0.001) improved brain antioxidant defense in a dose-dependent manner. Furthermore, AHE efficiently recused CisPT to induce DNA damage in brain tissue as revealed by ladder assay and DNA fragmentation patterns. Histopathological findings revealed severe neurodegenerations in CisPT treated group, however, AHE treatment noticeably precluded morphological alterations and neuron damages induced by CisPT.ConclusionA. hydaspica AHE extract may be provided as a prospective adjuvant that precludes CisPT-induced neurotoxicity due to its radical scavenging and antioxidant potential.
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    46 AHE
    47 AHE treatment
    48 BackgroundCisplatin
    49 CP
    50 DNA damage
    51 DNA fragmentation pattern
    52 H2O2
    53 IL-6 expression
    54 IL6
    55 MDA
    56 TNF
    57 acetate extract
    58 acetate fraction
    59 acetylcholinesterase activity
    60 activity
    61 adjuvant
    62 administration
    63 adverse effects
    64 alterations
    65 antioxidant defense
    66 antioxidant enzymes
    67 antioxidant potential
    68 assays
    69 brain AChE activity
    70 brain acetylcholinesterase activity
    71 brain antioxidant defenses
    72 brain tissue
    73 cerebral hemispheres
    74 cisPt
    75 cisplatin
    76 content
    77 cytokines
    78 damage
    79 day 13
    80 days
    81 days of treatment
    82 defense
    83 diminution
    84 dose-dependent manner
    85 effect
    86 efficacy
    87 enzyme
    88 ethyl acetate extract
    89 ethyl acetate fraction
    90 expression
    91 extract
    92 findings
    93 fraction
    94 fragmentation patterns
    95 genotoxicity
    96 group
    97 group II
    98 group IV
    99 hemisphere
    100 histopathological findings
    101 injection
    102 inoculation
    103 manner
    104 markers
    105 model
    106 morphological alterations
    107 neurodegeneration
    108 neuron damage
    109 neurotoxicity
    110 outcomes
    111 patterns
    112 potential
    113 pro-inflammatory cytokines
    114 prospective adjuvant
    115 reversal
    116 rodent models
    117 severe neurodegeneration
    118 silymarin
    119 tissue
    120 tissue MDA
    121 tissue TNF
    122 treatment
    123 treatment groups
    124 water
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