## 4 Discussion  
Overall, the current study supported the independent and combined health-promoting effects of MPE and CRE as nutritional treatments that may be preventive against the development of neurological and other chronic disorders. While serotonin and glutamate levels were unaffected by single or combined treatments with MPE and CRE, dopamine levels were significantly higher in the three treated groups compared to the control, with the combined effects having the greatest effect. It is well accepted that besides eating a balanced diet, several potential dietary interventions may help increase dopamine levels, including prebiotics, probiotics, fish oil, and vitamin D. This, in turn, could help mem brain function and mental health. Based on this, we could suggest that independent or combined MPE and CRE can induce healthier brain functions. This is in good agreement with the recent work of [PERSON] and [PERSON] [18], which reported that MPE and its bioactive xanthones are promising candidates for the treatment of Alzheimer's disease (AD), Parkinson's disease (PD), and depression. Moreover, it could find support in the previous work of [PERSON] et al. [19], which proved that CRE has demonstrated--a potency in modulating neurotransmitter levels--inflammatory signaling and excitotoxicity in the brain. This may support the hypothesis that MPE and curcumin, taken alone or in combination, may prevent the onset of dementia with Lewy bodies (DLB), the second-most common kind of late-onset degenerative dementia that is frequently associated with dopamine deficiency [20]. Under normal physiological conditions, a typical inflammatory response is characterized by the temporally limited elevation of inflammatory activity that occurs when a threat is present and resolves once the threat has passed [20; 21; 22]. However, the presence of \begin{table}
\begin{tabular}{c c c c c} \hline \hline
**Parameters** & **Groups** & **Mean \(\pm\) S.D.** & **Percent Change** & \(p\)**Value** \\ \hline \multirow{3}{*}{MDA} & Control & \(108.95\pm 12.54\) & \(100.00\) & \multirow{3}{*}{0.193} \\  & MPE & \(100.18\pm 0.98\) & \(-8.05\) & \(0.193\) \\ \(\mu\)m/ml & CRE & \(94.77\pm 812\) & \(-13.01\) & \(0.067\) \\  & MPE + CRE & \(93.17\pm 11.36\) & \(-14.48\) & \(0.071\) \\  & Control & \(148.31\pm 36.42\) & \(100.00\) & \\ GSH & MPE & \(123.86\pm 15.53\) & \(-16.48\) & \(0.205\) \\ \(\mu\)g/ml & CRE & \(125.11\pm 16.23\) & \(-15.64\) & \(0.230\) \\  & MPE + CRE & \(162.51\pm 47.20\) & \(+9.57\) & \(0.060\) \\ \hline \hline \end{tabular}
\end{table} 
Table 4: Levels of serum MDA, GSH, GST and vit. C in the control, independent MPE or CRE, and combined-treated rats. \begin{table}
\begin{tabular}{c c c c c} \hline \hline
**Parameters** & **Groups** & **Mean \(\pm\) S.D.** & **Percent Change** & \(p\)**Value** \\ \hline \multirow{3}{*}{CHOL/HDL-C} & Control & \(1.52\pm 0.28\) & \(100.00\) & \multirow{3}{*}{0.193} \\  & MPE & \(1.49\pm 0.24\) & \(-1.71\) & \(0.877\) \\ mg/dL & CRE & \(1.73\pm 0.40\) & \(+14.23\) & \(0.352\) \\  & MPE + CRE & \(1.36\pm 0.32\) & \(-10.67\) & \(0.416\) \\  & Control & \(4.61\pm 1.21\) & \(100.00\) & \\ HDL-C/LDL-C & MPE & \(2.54\pm 1.02\) & \(-44.90\) & \(0.016\) \\  & CRE & \(1.95\pm 0.40\) & \(-57.71\) & \(0.009\) \\  & MPE + CRE & \(5.35\pm 1.43\) & \(+16.07\) & \(0.465\) \\  & Control & \(232.55\pm 74.67\) & \(100.00\) & \\ GLU (mg/dL) & MPE & \(154.43\pm 34.27\) & \(-33.59\) & \(0.076\) \\  & CRE & \(121.12\pm 8.90\) & \(-47.91\) & \(0.009\) \\  & MPE + CRE & \(162.08\pm 39.89\) & \(-30.30\) & \(0.117\) \\ \hline \hline \end{tabular}
\end{table} 
Table 5: Levels of serum CHOL/HDL-C, HDL-C/LDL-C, and GLU in the control, independent MPE or CRE, and combined-treated rats. certain social, psychological, environmental, and biological factors has been linked to the prevention of the resolution of acute inflammation and, in turn, the promotion of a state of low-grade systemic chronic inflammation (SCI) characterized by having higher circulating levels of cytokines.