1. Introduction

Perinatal encephalopathy (PE) represents a complex of neurometabolic syndromes of the central nervous system (CNS) arising during the perinatal period due to hypoxia, ischemia, or toxic exposure. With an incidence of 10-40% in newborns, PE is characterized by disturbances in neuronal energy metabolism, heightened oxidative stress, and increased lipid peroxidation, which activate cellular apoptosis and can lead to long-term neurodevelopmental delays. While synthetic neuroprotectors are commonly used, their potential for toxicity and side effects has driven interest in safer, natural alternatives [1,2,3,4,5,6,7,8].

Biologically active supplements based on plant extracts, such as "Asqov-1" and "Asataqov," are of particular interest. These supplements are enriched with B-group vitamins (B₁, B₃, B₆), vitamins A and C, and essential minerals like zinc, magnesium, and iron. Additionally, they contain polyphenols and flavonoids, which are known to neutralize free radicals, inhibit lipid peroxidation, and reduce inflammation. The key pathogenic mechanism in perinatal hypoxic encephalopathy is oxidative stress, marked by elevated malondialdehyde (MDA) and reduced activity of antioxidant enzymes like superoxide dismutase (SOD) and catalase (CAT). Therefore, this study aimed to comprehensively evaluate the antioxidant and neuroprotective effects of "ASQOV-1" and "ASATAKOV" in an AlCl₃-induced hypoxia rat model of PE, assessing their impact on oxidative stress markers, neuromotor and cognitive functions [9,10,11,12,13,14,15,16,17,18].

2. Materials and Methods

Thirty male Wistar rats weighing 150–200 g were used in this study. The animals were housed under standard laboratory conditions with a 12-hour light/dark cycle and free access to food and water. All experimental procedures were approved by the Institutional Animal Ethics Committee. The rats were randomly divided into five groups (n=6 per group) (Table 1).

Table 1. Experimental design and animal grouping

At the end of the treatment period, animals were euthanized, and brain tissue homogenates were prepared. The following biochemical parameters were measured using a UV-Vis spectrophotometer:

ü Malondialdehyde (MDA): A marker of lipid peroxidation, measured as nmol/mg protein.

ü Superoxide Dismutase (SOD): Antioxidant enzyme activity, measured in units/mg protein.

ü Catalase (CAT): Activity determined by the rate of hydrogen peroxide decomposition, expressed as µmol H₂O₂/min/mg protein.

Functional recovery was assessed using:

Ø Rotarod Test: To evaluate motor coordination and balance, measured as the time (seconds) the animal remained on the rotating rod.

Ø Morris Water Maze Test: To assess spatial learning and memory, measured as the latency time (seconds) to find the hidden platform.

Ø SF-36 Quality of Life Index: A generalized index (%) adapted for animals, based on activity, grooming, and exploratory behavior.

All data were expressed as Mean ± Standard Error of the Mean (SEM). Statistical comparisons between groups were performed using one-way analysis of variance (ANOVA) followed by a post-hoc Student's t-test. A p-value of less than 0.05 was considered statistically significant.

3. Results

As shown in Table 1, induction of PE with AlCl₃ caused significant oxidative stress. In the PE model group, MDA levels increased 2.7-fold compared to the healthy control group (p < 0.001), indicating enhanced lipid peroxidation. Concurrently, the activities of the antioxidant enzymes SOD and CAT were significantly reduced by 56% and 54%, respectively (p < 0.001), reflecting a compromised antioxidant defense system.

Treatment with both "Asataqov" and "Asqov-1" significantly mitigated these changes. MDA levels were reduced by approximately 49% and 53% in the Asataqov and Asqov-1 groups, respectively, compared to the untreated PE model group (p < 0.01). Furthermore, SOD and CAT activities in both treatment groups were restored to levels that were not statistically different from the healthy control group (p > 0.05), indicating a powerful antioxidant effect (Table 2).

Table 2. Effect of "Asataqov" and "Asqov-1" on oxidative stress markers in a rat model of perinatal encephalopathy

The functional improvements paralleled the biochemical findings (Table 2). The PE model group exhibited significant deficits in motor coordination and cognitive function. Their time on the rotarod decreased by 45% (p < 0.001), and their escape latency in the Morris water maze increased by over three-fold (p < 0.001) compared to controls. The SF-36 quality of life index also dropped significantly to 58% (p < 0.001).

In contrast, rats treated with "Asataqov" and "Asqov-1" showed marked improvement. Coordination time increased by 58-63% (p < 0.01), and cognitive performance improved by 51-57% (p < 0.01) compared to the untreated PE group. The SF-36 index was restored to 84% and 87% in the Asataqov and Asqov-1 groups, respectively, which were significantly higher than the PE model group (p < 0.01). The effect of "Asqov-1" was slightly superior to that of "Asataqov" across all measured parameters (Table 3).

Table 3. Effect of "Asataqov" and "Asqov-1" on functional outcomes in a rat model of perinatal encephalopathy

4. Discussion

The results of this study robustly confirm the antioxidant and neuroprotective properties of the "Asqov-1" and "Asataqov" supplements in a preclinical model of perinatal encephalopathy. The significant reduction in MDA levels in the treatment groups directly demonstrates their capacity to inhibit lipid peroxidation, a key downstream effect of oxidative stress. Simultaneously, the restoration of SOD and CAT activities suggests that these supplements do not just act as direct free radical scavengers but also help to rejuvenate the brain's endogenous enzymatic antioxidant defense system. These neurochemical improvements translated into meaningful functional recovery, as evidenced by the enhanced performance in both coordination and cognitive tests. This indicates that the supplements are capable of protecting the neural substrates underlying motor control, learning, and memory from hypoxic damage.

The observed effects are likely due to the synergistic action of the supplements' bioactive constituents. The presence of flavonoids like quercetin and apigenin in "Asataqov" is known to contribute to anti-inflammatory and neuroprotective effects by modulating cellular signaling pathways. In "Asqov-1," the combination of B-group vitamins and minerals such as magnesium, zinc, and phosphorus likely supports neuronal health by acting as cofactors for ATP synthesis, neurotransmitter production, and maintaining synaptic plasticity. The slightly better performance of the "Asqov-1" group may be attributable to its specific mineral composition. The safety profile of these supplements, with an LD₅₀ > 5000 mg/kg placing them in the practically non-toxic class (hazard class VI), further supports their potential for use in vulnerable populations like children.

5. Conclusions

This study provides compelling experimental evidence that the food supplements "Asataqov" and "Asqov-1" possess significant antioxidant and neuroprotective activities. In a rat model of perinatal encephalopathy, they effectively reduced oxidative stress, restored the activity of key antioxidant enzymes, and improved motor coordination and cognitive function. Their high biological activity, coupled with a demonstrated low toxicity profile, positions them as promising and safe natural adjuncts for the prevention and rehabilitation of perinatal encephalopathy and potentially other hypoxic or neurodegenerative conditions. Further clinical investigations are warranted to confirm their efficacy and safety in children with PE.

ACKNOWLEDGEMENTS

The authors would like to thank the staff of the biochemical laboratories at Andijan State University and Andijan State Medical Institute for their technical support.

Conflict of Interest

The authors declare no conflicts of interest.