Purpose <p><i>Antiaris toxicaria</i> (family Moraceae) has been used traditionally to manage various conditions such as convulsion and neuropathy. Although neuroinflammation has been studied for some time, it still poses a significant health challenge in our societies. The study investigated the anti-neuroinflammatory properties of <i>A. toxicaria</i> in mice.</p> Methods <p>The aqueous extract of <i>A. toxicaria</i> was prepared by maceration in distilled water for 5&#xa0;days, filtered, and concentrated under reduced pressure. Male C57BL/6 mice (20–25&#xa0;g) were assigned to groups randomly. Acute toxicity was assessed by administering <i>A. toxicaria</i> extract (100, 300, 1000&#xa0;mg/kg) orally to mice for 14&#xa0;days. Behavioural signs, mortality, and weight changes were recorded. Separate groups of animals were also pretreated with <i>A. toxicaria</i> extract (10, 30, or 100&#xa0;mg/kg) or dexamethasone before LPS (500&#xa0;μg/kg) induction for 5&#xa0;days. A behavioural analysis was conducted using the object recognition test (ORT), followed by ELISA to measure cytokine and nitric oxide (NO) levels, and qPCR to assess NF-κB and IκBα mRNA expression in brain tissue.</p> Results <p>A positive discrimination index as well as a decrease in the levels of cytokines and NO were used as indicators of anti-neuroinflammatory activity. The results obtained in the experiment showed that the aqueous <i>A. toxicaria</i> extract (10, 30, and 100&#xa0;mg/kg) produced a significant (<i>p</i> &lt; 0.0001) positive discrimination index in mice in the ORT. Levels of the IL-1β, IL-6, NO, and TNF-α also reduced significantly (<i>p</i> &lt; 0.0001) in mice upon extract administration. Extract pretreatment also significantly (<i>p</i> &lt; 0.0001) reduced NF-κB (p65) mRNA concentration while significantly (<i>p</i> &lt; 0.0001) increasing brain IκBα mRNA concentrations.</p> Conclusion <p><i>A. toxicaria</i> therefore possesses anti-neuroinflammatory activity involving modulation of NF-κB signalling.</p>

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Aqueous extract of Antiaris toxicaria alleviates LPS-induced neuroinflammation by modulating NF-κB signalling

  • Akwasi Oppong,
  • Abiba Adams,
  • Ronald Reeves Ankrah,
  • Fafali Xedzro,
  • Priscilla Kolibea Mante

摘要

Purpose

Antiaris toxicaria (family Moraceae) has been used traditionally to manage various conditions such as convulsion and neuropathy. Although neuroinflammation has been studied for some time, it still poses a significant health challenge in our societies. The study investigated the anti-neuroinflammatory properties of A. toxicaria in mice.

Methods

The aqueous extract of A. toxicaria was prepared by maceration in distilled water for 5 days, filtered, and concentrated under reduced pressure. Male C57BL/6 mice (20–25 g) were assigned to groups randomly. Acute toxicity was assessed by administering A. toxicaria extract (100, 300, 1000 mg/kg) orally to mice for 14 days. Behavioural signs, mortality, and weight changes were recorded. Separate groups of animals were also pretreated with A. toxicaria extract (10, 30, or 100 mg/kg) or dexamethasone before LPS (500 μg/kg) induction for 5 days. A behavioural analysis was conducted using the object recognition test (ORT), followed by ELISA to measure cytokine and nitric oxide (NO) levels, and qPCR to assess NF-κB and IκBα mRNA expression in brain tissue.

Results

A positive discrimination index as well as a decrease in the levels of cytokines and NO were used as indicators of anti-neuroinflammatory activity. The results obtained in the experiment showed that the aqueous A. toxicaria extract (10, 30, and 100 mg/kg) produced a significant (p < 0.0001) positive discrimination index in mice in the ORT. Levels of the IL-1β, IL-6, NO, and TNF-α also reduced significantly (p < 0.0001) in mice upon extract administration. Extract pretreatment also significantly (p < 0.0001) reduced NF-κB (p65) mRNA concentration while significantly (p < 0.0001) increasing brain IκBα mRNA concentrations.

Conclusion

A. toxicaria therefore possesses anti-neuroinflammatory activity involving modulation of NF-κB signalling.