Naringin Reduced the Density and Total Number of Aβ Plaques and Restored Memory Function and Volume of Hippocampal CA1 Area in Alzheimer’s Disease Model Rats: A Stereological Study

Alzheimer’s disease (AD), the most prevalent form of dementia worldwide, is characterized by memory impairment and the accumulation of tau and beta-amyloid (Aβ) plaques. Naringin, a flavonoid, has exhibited strong anti-inflammatory, anti-oxidant, and anti-apoptotic properties.

In this study, we aimed to demonstrate the neuroprotective effects of naringin on memory function, the total number and density of Aβ plaques, and the volume of the hippocampal CA1 region in a scopolamine (SCO)-induced AD model in rats.

Forty male Wistar rats were randomly divided into the following groups: A control group, a saline + SCO (3 mg/kg) group (pretreated with 200 µL saline), and 3 treatment groups receiving naringin at doses of 50 mg/kg/day + SCO, 100 mg/kg/day + SCO, and 200 mg/kg/day + SCO (pretreated with 50, 100, or 200 mg/kg of naringin) for 14 consecutive days via intraperitoneal (IP) injection. After the 14-day pretreatment period, the saline + SCO and 3 naringin treatment groups received SCO (3 mg/kg) to induce an AD-like condition. Memory function was assessed using the inhibitory passive avoidance test. Following brain harvesting, paraffin-embedded coronal brain slices were stained with Congo red, and the density and the total number of Aβ plaques and the volume of the hippocampal CA1 area were estimated using unbiased stereological techniques.

The results indicated that naringin significantly improved memory function, with the most pronounced effect observed in the naringin 200 mg/kg + SCO group. Stereological analysis revealed that SCO reduced the volume of the hippocampal CA1 area and increased the total number and density of Aβ plaques. Pretreatment with naringin significantly restored the hippocampal CA1 volume in the 200 mg/kg + SCO group compared to the saline + SCO group. Additionally, naringin reduced the total number and density of Aβ plaques, with the most significant decrease observed in the 200 mg/kg + SCO group.

Naringin restored memory function and the volume of the hippocampal CA1 region while reducing the total number and density of Aβ plaques in a SCO-induced AD model in rats. This stereological study complements previous molecular research on naringin’s neuroprotective effects in AD-like pathogenesis.