Swimming Training and Nanoformulation of Traditional Herbal Medicines Recovered Sensory-Motor Impairment by Modulating the Molecular Signaling Pathway in Rat Brain Tumor Models

Background: Glioblastoma (GBM) is one of the most aggressive tumors, health-threatening, and resistant to available treatment approaches for people worldwide. Objectives: This study aimed to evaluate effects of swimming training and a supplement comprising four nanoliposome herbal extracts in a rat model with mid-brain tumor. Methods: In this experimental study, 56-male-Wistar rats (230 ± 20 g) were divided into eight groups (n = 7): Normal group, model group, model + exe group, model + lipo, model + extract, model + lipo-extract, model + extract-exe, model + lipo-extract + exe. Mid-brain tumor model was induced by injection of the C6 glioma cell line (5 × 105 cell suspension) using stereotaxic techniques in the substantia nigra area of rats. Consumption of nanoformulation of herbals extract (100 mg/kg/day), crude extract (100 mg/kg/day), and swimming training (30 min, 3 days/week) were performed for six weeks. P53, Hras, IL-10, and Casp8 were studied by bioinformatics analysis. We assessed the relative expression of genes in the mid-brain tumor via the quantitative Real-Time PCR (qRT-PCR) method. Beam test and sciatic functional index assessed nerve function and motor coordination. Results: In-silico analysis highlighted substantial genes with significant differential expression compared to healthy status as biomarkers in pathogenesis conditions. The expression level of the P53 and Hras increased with swimming training and nanoliposomes enriched complex complement. Besides, the expression of the IL-10 and Casp8 decreased with swimming training and nanoliposomes enriched complex complement. Conclusions: Our findings show that swimming training and nanoliposome-enriched combined supplements in rats can possibly be considered effective complementary medicine for motor impairment recovery induced by the brain tumor in the substantia nigra area.