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Advanced Neurology                                             Pantothenic acid in kainic acid-induced epilepsy




            Table 1. Effect of pantothenic acid on various biochemical parameters in kainic acid‑induced epilepsy in mice
             Group  AChE (nmol·min ·mL ·g    GSH (nM/mg   TBARS (nM/  Nitrite (nM/  SOD (IU/mg   Catalase (μM of H O   2
                                    −1
                                  −1
                               −1
                                                                                                     2
                         of tissue)     of protein)  mg of protein)  mg of protein)  of protein)  decomposition·min ·mg of protein)
                                                                                                 −1
            1            3.2±0.853       7.37±0.13  1.31±0.05   1.19±0.08  37.3±1.05         1.18±0.076
            2            6.7±0.73 ###    2.9±0.92 ###  3.72±0.32 ###  3.37±0.91 ###  9.52±1.2 ###  0.36±0.07 ###
            3           4.89±0.19***    5.86±0.89***  2.56±0.98***  2.04±0.76***  33.73±2.03***  0.91±0.71***
            4            6.55±0.75*      4.67±1.32*  3.09±0.98*  3.17±0.97*  13.72±1.76*     0.47±0.08*
            5            5.89±0.7**      5.98±0.7**  2.68±0.4**  3.09±0.3**  21.73±1.8**    0.79±0.04**
            6            4.53±0.8***    7.1±0.54***  1.94±0.8***  1.93±0.7***  31.36±2.17***  0.97±0.06***
            Data are expressed as means±standard error of the mean, n = 6. Data were analyzed using one-way analysis of variance followed by Tukey-Kramer
            multiple comparisons test. *P < 0.05, **P < 0.01, ***P < 0.001, compared with vehicle-treated KA group (i.e., Group 2).  P < 0.001, compared with
                                                                                        ###
            control group (i.e., Group 1). Group 1: control group, Group 2: Vehicle-treated KA group consisting of untreated KA-induced mice, Group 3: Group
            of diazepam-treated KA-induced mice, Group 4: Group of pantothenic acid (30 mg/kg, p.o.)-treated KA-induced mice, Group 5: Group of pantothenic
            acid (60 mg/kg, p.o.)-treated KA-induced mice, and Group 6: Group of pantothenic acid (90 mg/kg, p.o.)-treated KA-induced mice. AChE
            acetylcholine esterase, GSH: Glutathione, SOD: Superoxide dismutase, TBARS: Thiobarbituric acid reactive substances
            3.5. Effect of PA on GSH levels in KA-induced SE in mice

            Brain GSH levels were measured in the control, vehicle-
            treated  KA-induced,  and  PA  -treated  mice.  GSH  levels
            were found to be lower (2.9 ± 0.92 nM/mg of protein)
            in the vehicle-treated KA group (P < 0.001) than in the
            control group (7.37 ± 0.13 nM/mg of protein). GSH levels
            were 4.67 ± 1.32, 5.98 ± 0.7, and 7.1 ± 0.54 nM/mg of
            protein in the mice treated with PA at 30, 60 and 90 mg/kg
            (i.p.), respectively. Furthermore, the levels were found to
            be maximum in animals treated with the dose of 90 mg/kg
            as compared to KA-treated Group 2 (P < 0.001, Table 1).

            3.6. Effect of PA on TNF-α level in KA-induced SE in mice
              The brain levels of TNF-α were significantly
            increased after KA administration as compared to level   Figure 3. Effect of 7-day pretreatment with pantothenic acid on TNF-α
                                                               level in KA-induced SE in mice. Data are expressed as means ± standard
            found  in  the  control  group  (804.09  ±  19.02  pg/mL  and   error of the mean,  n = 6. Data were analyzed using one-way analysis
            481.31 ± 7.67 pg/mL, respectively, P < 0.001). PA treatment   of variance followed by Tukey-Kramer multiple comparisons test.
            caused a dose-dependent reduction in brain levels of   *P<0.05, **P<0.01, ***P<0.001, compared with vehicle-treated KA group.
            TNF-α (Figure 3), with the highest inhibition occurred at   ### P<0.001, compared with control group.
            the dose of 90 mg/kg (P < 0.001).
                                                               and MAO-B by 21% and 35%, respectively, and PA
            3.7. Effects on body and brain weight              (90 mg/kg, p.o.) resulted in significant inhibition of both
            The mice body weight and brain weight decreased in   MAO isoforms by 35% and 65%, respectively (Table 3).
            KA-induced mice, whereas other groups also showed
            changes in size and body weight. Mice treated with PA   3.9. Histopathological changes in brain tissue
            improved the hypotrophy of their brains caused by KA   From the histopathological study, it was observed that
            induction in the absence of interventional treatment   the normal control group or Group 1 (Figure 4A) showed
            (Table 2).                                         a normal brain parenchyma with normal neuronal
                                                               morphology. KA-treated mice  in Group  2 (Figure  4B)
            3.8. Effect of PA on MAO-A and MAO-B levels        showed neuronal degradation in the brain parenchyma,
            The effects of PA on the MAO concentration are     small  pyknotic  nuclei,  and  extracellular  eosinophilic
            shown in  Table 3. The MAO-A and MAO-B activity    deposition. In the standard group or Group 3 (Figure 4C),
            levels of the control group were 26.1 ± 0.32 and   animals showed mild changes in neuronal degeneration,
            23.2 ± 0.24 nmol/mg of protein, respectively. Oral (p.o.)   and many nuclei were pyknotic and closely packed. The
            administration of 60  mg/kg PA inhibited MAO-A     mice in Group 4 (Figure 4D) and Group 5 (Figure 4E),



            Volume 1 Issue 2 (2022)                         5                        https://doi.org/10.36922/an.v1i2.40
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