Objective. To compare the changes of chemical components of Hedysari Radix (HR) before and after honey-processing, and to explore the material basis of the difference between HR and honey-processed Hedysari Radix (HPHR) in Buzhong Yiqi. Methods. Different compounds in aqueous extracts of HR and HPHR were analysed by UPLC-MS. A rat model of spleen qi deficiency was established. The rats were treated with different doses of water extracts of HR or HPHR, and pathological differences in spleen tissue, serum levels of D-xylose, gastrin (GAS) and amylase (AMS) interleukin-2 (IL)-2 and tumour necrosis factor-α (TNF-α), as well as spleen and thymus indices, were used as indicators. Differences in the efficacy of HR and HPHR in Buzhong Yiqi were studied. Results. The research showed that compared with the blank group, the spleen tissue of rats in the model group showed spleen tissue damage, which mainly manifested as unclear boundaries between red pulp and white pulp, irregular spleen morphology and irregular arrangement, and the structure of white pulp destruction, less lymphocytes, the number of germinal centers decreased or atrophied. Compared with the model group, the middle and high dose groups of HR and HPHR had protective effects on spleen tissue of spleen-qi deficiency rats, and HPHR had a stronger effect; compared with those in the model group, rats in each treatment group showed remarkably higher serum D-xylose, GAS and AMS levels and thymus and spleen indices, and remarkably lower serum IL-2 and TNF-α levels, among which HPHR group showed better regulation effect than HR group. A total of 16 differential compounds were found in the aqueous extracts of HR and HPHR, of which 10 compounds in HPHR were up regulated, while 6 compounds were down regulated compare to HR. Conclusion. The results indicated that both HR and HPHR can improve spleen qi deficiency syndrome of rats, the pharmacodynamic effect of the latter was better than the former. Differences in components of HR and HPHR potentially leading to variations in efficacy.

Inflammation is the primary pathological feature of neurodegenerative diseases such as Alzheimer’s disease (AD) and Parkinson’s disease. Proinflammatory molecules (e.g., S100A9) play important roles during the progression of the diseases by regulating behavior and fate of multiple cell types in the nervous system. Our earlier studies reveal that S100A9 is toxic to neurons, and its interaction with Aβ peptides leads to the formation of large nontoxic amyloidogenic aggregates, suggesting a protective role of coaggregation with Aβ amyloids. We herein demonstrate that S100A9 interacts with neural stem cells (NSCs) and causes NSC differentiation. In the brain of transgenic AD mouse models, we found large quantities of proinflammatory S100A9, which colocalizes with the differentiated NSCs. NSC sphere formation, which is a representative character of NSC stemness, is also substantially inhibited by S100A9. These results suggest that S100A9 is a representative marker for the inflammatory conditions in AD, and it promotes NSC differentiation. Intriguingly, in contrast to the death of both stem and differentiated NSCs caused by high S100A9 doses, S100A9 at a moderate concentration is toxic only to the early differentiated NSCs but not the stem cells. We therefore postulate that, at the early stage of AD, the expression of S100A9 leads to NSC differentiation, which remedies the neuron damage. The application of drugs, which help maintain NSC stemness (e.g., the platelet-derived growth factor, PDGF), may help overcome the acute inflammatory conditions and improve the efficacy of NSC transplantation therapy.

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