Caffeoylquinic acids (CQAs) are main constituents in many herbal medicines with various biological and pharmacological effects. However, CQAs will degrade or isomerize when affected by temperature, pH, light, etc. In this study, high-performance liquid chromatography with photodiode array detection (HPLC-PDA) and high-performance liquid chromatography tandem mass spectrometry (HPLC-MS/MS) was utilized to study the stability and degradation of CQAs (three mono-acyl CQAs and four di-acyl CQAs) under various ordinary storage conditions (involving different temperatures, solvents, and light irradiation). The results indicated that the stability of CQAs was mainly affected by temperature and light irradiation, while solvents did not affect it in any obvious way under the conditions studied. Mono-acyl CQAs were generally much more stable than di-acyl CQAs under the same conditions. Meanwhile, the chemical structures of 30 degradation products were also characterized by HPLC-MSⁿ, inferring that isomerization, methylation, and hydrolysis were three major degradation pathways. The result provides a meaningful clue for the storage conditions of CQAs standard substances and samples.

Realgar and indigo naturalis are clinically combined to treat varieties of leukemia. Exploring the drug‐drug interactions might be beneficial to find active substances and develop new targeted drugs. This study aimed at exploring the change of arsenic concentration in mice and across MDCK‐MDR1 cells and the cytotoxicity on K562 cells when realgar and indigo naturalis were combined. In the presence or absence of indigo naturalis, pharmacokinetics and cell‐based permeability assays were used to evaluate the change of arsenic concentration, and K562 cell line was applied to evaluate the change of cytotoxicity. The drug concentration‐time profiles exhibited that the combination medication group generated higher AUC, t_half, and longer MRT for arsenic, compared with the single administration of realgar. The apparent permeability coefficients (P_app) of bidirectional transport in MDCK‐MDR1 cell permeability experiments showed that arsenic permeability obviously went up when indigo naturalis was incubated together. The combination medication significantly decreased the cell viability of K562 cells when both the concentration of realgar and the concentration of indigo naturalis were nontoxic. The pharmacokinetic research, the MDCK‐MDR1 based permeability study, and the K562 cytotoxicity study were united together to verify the combination medication of realgar and indigo naturalis enhanced the absorption and the permeability across cells for arsenic and effectively inhibited the proliferation of K562 cell line. The molecular binding of As₄S₄ and indirubin was analyzed by computational study. It is predicted that the formation of the complex [As₄Indirubin] involves noncovalent interaction that changes the concentration of arsenic.

Alzheimer’s disease (AD) is a neurodegenerative disease and threatens the health of the aged population worldwide. In the present study, we investigated cognitive improvement by aloe emodin in aluminum‐induced AD rats. We orally administered aluminum chloride (150 mg/kg) to Sprague–Dawley rats for 8 weeks to induce AD. In the 5th to the 8th week, the rats were injected intraperitoneally with AE (5, 10, and 15 mg/kg). Behavioral, histopathological, and biochemical assessments were performed. The results showed that AE alleviated cognitive impairment in aluminum‐induced AD rats and inhibited aluminum‐induced hippocampal neuronal damage. Furthermore, aloe emodin relieved the aluminum burden in the brain of aluminum‐induced AD rats, attenuated the aluminum‐induced increase in Aβ₄₂ level and acetylcholinesterase activity, and reduced the levels of tumor necrosis factor‐α, interleukin‐6, interleukin‐1α, and interleukin‐1β. These effects suggest that the mechanism by which AE alleviates AD‐related cognitive impairment is by removal of excess aluminum, decreasing Aβ₄₂ deposition, regulating the cholinergic system, and reducing neuroinflammation.