Abstract
Sodium valproate (SVPA) is indicated for the management of partial and generalized epilepsy with major limitation of pan-toxicity. Musanga cecropioides stem-bark (MCS) is used in ethnomedicine for multiple health benefits. The aim of the study was to test the ameliorative effect of MCS extract on SVPA-induced damage in rodent. The rats were administered with SVPA (500 mg/kg b.w. followed by MCS (50, 100, and 200 mg/kg b.w.) and reference drug, vinpocetine (25 mg/kg b.w.) orally and sub-acutely. The protective effects of MCS extract on their weights, hematological, biochemical, lipid, kidney and electrolytes profiles parameters were examined. Following rats sacrifice, the liver, kidney and lungs were subjected to histopathological analysis. The study indicated that SVPA significantly up-regulated the liver function enzymes (P< 0.001), lipid profile (P< 0.01-0.001), kidney function (P< 0.05–0.01) and electrolytes (P< 0.01–0.001) biomarkers and elicited gross alterations of measured indices. However, this effects were dose dependently reversed by MCS extract with higher hepatoprotective percentages, for liver enzymes (77-261%), lipid profiles (74–133%), electrolytes (59-169%) and kidney function (82–154%) compare to vinpocetine values of 63–103%, 80- 127%, 70–161% and 27-78%, respectively. No significant alteration in hematology and relative organ weights. The effect on histopathology corroborated biochemical study. Vinpocetine exhibit no therapeutic effect on the histopathological alteration of liver and kidney but only on the lungs. The presence of potential active ingredients in MCS extract confirms it as an alternative adjunctive therapy in abrogating SVPA – induced pan-toxicity derangement in rats.
Highlights
Valproic acid (2‐propylpentanoic acid) is a branched short chain fatty acid derived from naturally occurring valeric acid extracted from Valeriana officinalis [1, 2], but it was first synthesized in 1882 [3]
The low permeability of SVPA to the brain necessitates a relatively high daily dosage which posit adverse effects such as bone marrow suppression [16], lethargy [5], hepatotoxicity [17], nephrotoxicity [18], teratogenicity and developmental toxicity [19, 20], neurotoxicity [21], hematotoxicity [22], pancreatitis [23], and numerous idiopathic effects which in the offspring might lead to autistic spectrum disorder [24, 25]
The major limitation of SVPA are its side effects varying from sedation, fatigue, tremor, gastrointestinal symptoms, weight gain [27, 28], long‐term adverse symptoms associated with SVPA are metabolic disorders such as hyperinsulinemia, insulin resistance, hyperleptinemia and leptin resistance resulting in weight gain, dyslipidemia, menstrual irregularities, hyperandrogenism and polycystic ovarian syndrome [29]
Summary
Valproic acid (2‐propylpentanoic acid) is a branched short chain fatty acid derived from naturally occurring valeric acid extracted from Valeriana officinalis [1, 2], but it was first synthesized in 1882 [3]. The esterified product of valproic acid, sodium valproate (SVP) is the highly prescribed drug treatment for partial and generalized epilepsy globally [5], and used primarily in the management of a number of pathologies, seizures, bipolar disorder, mood, anxiety. The low permeability of SVPA to the brain necessitates a relatively high daily dosage which posit adverse effects such as bone marrow suppression [16], lethargy [5], hepatotoxicity [17], nephrotoxicity [18], teratogenicity and developmental toxicity [19, 20], neurotoxicity [21] , hematotoxicity [22], pancreatitis [23], and numerous idiopathic effects which in the offspring might lead to autistic spectrum disorder [24, 25]. Carnitine is prescribed officially to mitigate the adverse effects of SVPA [30]
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