The purpose of this study was to investigate the protective effect of chitooligosaccharide (COS) against alcohol-induced oxidative stress injury and neuronal cell apoptosis in the brain of neonatal rats. In total, 56 neonatal SD rats were randomly divided into four groups: normal control (NC), COS, model (MOD), and COS + MOD. The effect of COS on body mass change, histopathology, oxidative stress injury and the expression of apoptosis-associated proteins was evaluated. The results showed that oral administration of alcohol slowed down body mass gain and caused necrosis and deformation of brain nerve cells, but this effect was relieved by intervention with COS. Additionally, intervention with COS increased the levels of superoxide dismutase (SOD) activity, glutathione (GSH) content and total antioxidant capacity (T-AOC), and significantly reduced malondiadehyde (MDA) level in brain tissue. COS significantly relieved oxidative stress damage caused by ethanol exposure in the brain of neonatal rats, and reduced the expression of cleaved caspase-3. These results indicated that COS protects against brain damage induced by ethanol in neonatal rats, and the underlying mechanism may be related to the fact that COS can alieve ethanol-induced oxidative stress injury of brain tissue and inhibit neuronal cell apoptosis.

Fluorescent probe labeling is easy to operate and the sensitivity of fluorescence detection is 3–4 orders of magnitude higher than traditional methods such as ultraviolet visible (UV-Vis) spectroscopy. The absorption and distribution of chitosan oligosaccharide (COS) monomers with different degrees of polymerization (DPs) in mice was analyzed by fluorescent probe labeling. In this study, we analyzed the differences in the absorption and distribution of COS monomers with DPs of 2–5 in mice gavaged with fluorescein isothiocyanate (FITC) labeled COS monomers through fluorescence signal detection by a small animal intravital optical imaging system and fluorescence quantification. The results showed that at 1 h after administration, the fluorescence signal in the mice reached its peak level. COS could be absorbed into the blood and cross the blood-brain barrier to distribute into the brain tissue. COS mainly distributed into the kidney and liver, followed by the heart and spleen, and a small amount of COS distributed into the lung and brain. The distribution of COS monomers in the kidney and liver was positively correlated with the DP, while the peak distribution in serum, heart, spleen, lung, and brain in decreasing order was as follows: chitobiose > chitotetraose > chitotriose > chitopentose. The findings of this study are meaningful for guiding future study of the structure-activity relationship of functional COS and provide a reference for further study of the functional mechanism of COS, which will accelerate the development and application of COS in functional foods.