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Silibinin is a flavonoid extracted from the medicinal plant Silybum marianum (milk thistle), traditionally used to treat liver disease. Recent studies have shown that the antioxidative stress and anti-inflammatory effects of milk thistle are used in the treatment of neurological diseases. Silibinin has antioxidative stress and antiapoptotic effects and reduces cognitive impairment in models of Alzheimer’s disease (AD). However, the underlying mechanism of silibinin related to improvement of cognition remains poorly understood. In this study, we used the model of lateral ventricle injection of formaldehyde to examine the related mechanism of silibinin in improving cognitive impairment disorders. Oral administration of silibinin for three weeks significantly attenuated the cognitive deficits of formaldehyde-induced mice in a Y -maze test and Morris water maze test. Y -maze results show that silibinin increases the rate of spontaneous response alternation in FA-induced mice. Silibinin increases the target quadrant spending time and decreases escape latency in the Morris water maze test. We examined the effect of silibinin on the NRF2 signaling pathway, and silibinin promoted the nuclear transfer of NRF2 and increased the expression of HO-1 but did not significantly increase the protein expression of NRF2 in the hippocampus. Well, silibinin reduces the content of DHE and decreases the levels of apoptosis of mature neuron cells. We investigated the effect of silibinin on the content of formaldehyde degrading enzymes; biochemical analyses revealed that silibinin increased GSH and ALDH2 in formaldehyde-induced mice. In addition, as one of the pathological changes of AD, TAU protein is also hyperphosphorylated in FA model mice. Silibinin inhibits the expression of GSK-3β in model mice, thereby reducing the phosphorylation of TAU proteins ser396 and ser404 mediated by GSK3β. Based on our findings, we verified that the mechanism of silibinin improving cognitive impairment may be antioxidative stress, and silibinin is one of the potentially promising drugs to prevent formaldehyde-induced cognitive impairment.

By means of collision models (CMs) where the environment is simulated by a collection of ancillas consisting of two entangled qubits, we investigate the effects of entanglement in the environment on the non-Markovianity of an open quantum system. Two CMs are considered in this study, in the first one the open quantum system S directly collides with the environment, while in the second one the system interacts with two intermediate qubits which, in turn, are coupled to the environment. We show that it is possible to enhance the non-Markovianity by environment entanglement in both models. In particular, in the second model, we show that the initial state of the auxiliary qubits can also affect the non-Markovianity of the system and there exists the optimal combination of the initial environmental state and the initial state of auxiliary qubits. In this case, the non-Markovianity can be greatly enhanced.

By means of composite quantum collision models, we study the entanglement dynamics of a bipartite system, i.e., two qubits S 1 and S 2 interacting directly with an intermediate auxiliary qubit S A, while S A is in turn coupled to a thermal reservoir. We are concerned with how the intracollisions of the reservoir qubits influence the entanglement dynamics. We show that even if the system is initially in the separated state, their entanglement can be generated due to the interaction between the qubits. In the long-time limit, the steady-state entanglement can be generated depending on the initial state of S 1 and S 2 and the environment temperature. We also study the dynamics of tripartite entanglement of the three qubits S 1, S 2, and S A when they are initially prepared in the GHZ state and separated state, respectively. For the GHZ initial state, the tripartite entanglement can be maintained for a long time when the collision strength between the environment qubits is sufficiently large.