Senile insomnia is a common clinical disorder. Traditional Chinese medicine （TCM） primarily attributes the pathogenesis of insomnia to Yang failing to enter Yin aspect and disharmony between Yin and Yang. However， the discussion on insomnia caused by Yang Qi deficiency in elderly patients remains insufficient. According to the theory of extreme Yang in the Huang Di Nei Jing， this paper systematically elucidates the central role of Yang Qi in maintaining mental tranquility and regulating the sleep-wake cycle. It posits that the natural decline of Yang Qi with aging leads to Yang failing to enter Yin aspect or deficient Yang floating upward， which constitutes a key pathogenesis of senile insomnia. From a modern medical perspective， mitochondrial energy metabolism dysfunction is identified as a crucial biological basis. Mitochondrial functional declines result in insufficient adenosine triphosphate （ATP） production and reactive oxygen species （ROS） accumulation， which disrupts the synthesis of sleep-related neurotransmitters and the expression of circadian clock genes， ultimately leading to sleep disturbances. Furthermore， this sutdy explores the intrinsic connection between Yang Qi deficiency and mitochondrial dysfunction， arguing for a high degree of correspondence in their functional and pathological manifestations. Accordingly， the therapeutic principle of warming and tonifying Yang Qi， nourishing the heart and tranquilizing the mild is proposed. This approach employs Yang-warming formulas and acupuncture to regulate the mitochondrial function through multiple targets. Specific mechanisms include enhancing the activity of respiratory chain complexes， activating the mitochondrial autophagy， and mitigating oxidative stress， thereby restoring energy metabolic homeostasis and improving sleep in the elderly. This study provides a new theoretical foundation and a therapeutic strategy for integrating TCM and Western medicine in preventing and treating senile insomnia.

ObjectiveTo investigate the mechanism by which Anmei Dan （AMD） regulates recombinant sirtuin 3/nuclear factor erythroid 2-related factor 2（SIRT3/Nrf2） signaling to ameliorate mitochondrial oxidative stress and improve the cognitive function in aged sleep-deprived mice. MethodsSixty aged C57 mice were randomly assigned to a control group， a model group， a melatonin （1.3 mg·kg^-1·d^-1） group， and high-， medium-， and low-dose （26.26， 13.13， 6.565 g·kg^-1·d^-1， respectively） AMD groups， with ten mice per group. Continuous sleep deprivation was administered for 4 weeks via a custom-built sleep deprivation chamber. The cognitive function of mice was assessed via the Morris water maze test. Hematoxylin-eosin （HE） staining was performed to observe morphological alterations in pyramidal neurons. Biochemical assays were carried out to measure the hippocampal and serum levels of superoxide dismutase （SOD）， malondialdehyde （MDA）， glutathione peroxidase （GSH-Px）， catalase （CAT）， and total antioxidant capacity （T-AOC）. Transmission electron microscopy was adopted to examine mitochondrial pathological alterations in the hippocampus. Immunohistochemical assay was conducted to examine the expression of nuclear factor E₂-related factor 2 （Nrf2）， sirtuin 3 （SIRT3）， peroxisome proliferator-activated receptor gamma coactivator-1α （PGC-1α）， mitochondrial transcription factor A （TFAM）， and brain-derived neurotrophic factor （BDNF） in the mouse hippocampus. The protein levels of Nrf2， SIRT3， heme oxygenase-1 （HO-1）， and NAD（P）H：quinone oxidoreductase 1 （NQO1） in mouse hippocampal tissue were determined by Western blot. Immunofluorescence double labeling was employed to determine the protein levels of SIRT3/Nrf2 in mouse hippocampal tissue. ResultsCompared with the control group， the model group exhibited prolonged latency to navigate， increased total swimming distance， reduced number of platform crossings， and shortened time spent in the target quadrant （P<0.05， P<0.01）， disorganized morphology and arrangement of hippocampal neurons， with increased damaged mitochondria， mitochondrial swelling， reduced cristae， and vacuolization， declined levels of SOD， GSH-Px， CAT， and T-AOC and elevated levels of MDA in the hippocampus and serum （P<0.01）， and downregulated protein levels of SIRT3， Nrf2， PGC-1α， TFAM， BDNF， HO-1， and NQO1 （P<0.01）. Compared with the model group， the melatonin group and AMD groups exhibited shortened spatial navigation latency， reduced total swimming distance， increased number of platform crossings， and prolonged activity time in the target quadrant （P<0.05， P<0.01）， reduced neuronal damage and mitochondrial damage in the hippocampal tissue， declined level of MDA and elevated levels of SOD， GSH-Px， CAT， and T-AOC in the hippocampus and serum （P<0.05， P<0.01）， and upregulated protein levels of SIRT3， Nrf2， PGC-1α， TFAM， BDNF， HO-1， and NQO1 in the hippocampus （P<0.05， P<0.01）. ConclusionAMD may improve the learning and memory in aged sleep-deprived mice by mediating mitochondrial oxidative damage through the SIRT3/Nrf2 signaling pathway.

ObjectiveTo investigate the effects of Anmei Dan （AMD） on the expression of proteins in the C-X3-C motif chemokine ligand 1 （CX3CL1）/C-X3-C chemokine receptor 1 （CX3CR1） signaling pathway， hippocampal inflammation， and learning and memory in an aged sleep-deprived model. MethodsSixty aged C57 mice were randomly assigned into a control group， a model group， a melatonin group （1.3 mg·kg^-1·d^-1）， and high-， medium-， and low-dose AMD groups （26.26， 13.13， 6.565 g·kg^-1·d^-1， respectively）， with 10 mice per group. Continuous sleep deprivation was administered for 4 weeks through a custom-built sleep deprivation chamber. The cognitive function of mice was assessed via the Y-maze test. Histomorphological alterations in pyramidal cells of the hippocampal CA1 and DG regions were examined by hematoxylin-eosin （HE） and Nissl staining. Synaptic morphology in the hippocampus was visualized with Golgi staining. Enzyme-linked immunosorbent assay （ELISA） was employed to measure the levels of inflammatory cytokines interleukin-1β （IL-1β）， interleukin-6 （IL-6）， and tumor necrosis factor-α （TNF-α） in the hippocampal tissue as well as the level of interleukin-10 （IL-10） in the prefrontal cortex. Real-time PCR was performed to detect markers of M1-type ［cluster of differentiation （CD） 86 and inducible nitric oxide synthase （iNOS）］ and M2-type ［CD206 and arginase 1 （Arg1）］ macrophages. Western blot was employed to quantify the protein levels of CX3CL1， CX3CR1， phosphorylated nuclear factor κB p65 subunit （p-NF-κB p65）， and phosphorylated p38 mitogen-activated protein kinase （p-p38 MAPK） in the hippocampus. Immunofluorescence double staining was performed to co-label CX3CR1 with ionized calcium-binding adapter molecule 1 （Iba-1） for observation of the co-localization of target proteins with microglia. ResultsCompared with the control group， the model group exhibited disrupted daily activity patterns with reduced spontaneous alternation rates （P<0.01）， disorganized morphology and arrangement of hippocampal neurons， accompanied by reduced numbers of Nissl bodies and dendritic spines （P<0.01）， upregulated protein levels of IL-6， IL-10， IL-1β， TNF-α， CX3CL1， CX3CR1， p-NF-κB p65， p-p38 MAPK， and Iba-1 and mRNA levels of CD86 and iNOS （P<0.01）， and downregulated mRNA levels of CD206 and Arg1 （P<0.05，P<0.01）. Compared with the model group， the melatonin group and medium- and high-dose AMD groups showed increased spontaneous alternation rates （P<0.01）， improved neuronal morphology， number， and spine density in the hippocampal CA1 and DG regions （P<0.01）， declined levels of IL-6， IL-10， IL-1β， and TNF-α （P<0.05， P<0.01）， downregulated protein levels of CX3CL1， CX3CR1， p-NF-κB p65， p-p38 MAPK， and Iba-1 and mRNA levels of CD86 and iNOS， and upregulated mRNA levels of CD206 and Arg1 （P<0.01）. ConclusionAMD may improve the learning and memory in aged sleep-deprived mice by mediating neuroinflammation through the CX3CL1/CX3CR1 signaling pathway.

OBJECTIVE: To observe the effects of electroacupuncture (EA) on improving motor function and regulating microglial activation based on Notch receptor 1 (Notch1)/Hes family bHLH transcription factor 1 (Hes1) pathway in mice with Parkinson's disease (PD). METHODS: Thirty-six male C57BL/6 mice were randomly divided into a control group, a model group and an EA group, 12 mice in each group. PD model was established by intraperitoneal injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) for 7 consecutive days in the model group and the EA group. From the 1st day of modeling, EA was applied at "Baihui" (GV20) and bilateral "Shenshu" (BL23) in the EA group, with continuous wave, in frequency of 2 Hz and current of 2 mA, 15 min a time, once a day for 14 days continuously. The behavioral performance was evaluated by gait test, pole climbing test and hanging test, the number of positive cells of tyrosine hydroxylase (TH) and the co-expression positive cells of Notch1/ionized calcium binding adaptor molecule 1 (Iba-1) in the substantia nigra of midbrain was assessed by immunofluorescence, the protein expression of TH, α-synuclein (α-syn), Notch1, Hes1, Iba-1, inducible nitric oxide synthase (iNOS), Arginase-1 (ARG1), tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6 and IL-10 was detected by Western blot, the mRNA expression of Notch1 and Hes1 was detected by real-time PCR. RESULTS: Compared with the control group, in the model group, the stride frequency was accelerated (P<0.001) and the stride length was shortened (P<0.001) for the four limbs, the pole climbing test time was prolonged (P<0.01) and the grip level was reduced (P<0.01); in the substantia nigra of midbrain, the number of positive cells of TH was decreased (P<0.001), the number of co-expression positive cells of Notch1/Iba-1 was increased (P<0.001), the protein expression of α-syn, Notch1, Hes1, Iba-1, iNOS, TNF-α, IL-1βand IL-6 was increased (P<0.01, P<0.05, P<0.001), the protein expression of TH, ARG1 and IL-10 was decreased (P<0.01, P<0.001), the mRNA expression of Notch1 and Hes1 was increased (P<0.01). Compared with the model group, in the EA group, the stride frequency was decelerated (P<0.001) and the stride length was increased (P<0.05, P<0.01, P<0.001) for the four limbs, the pole climbing test time was shortened (P<0.05) and the grip level was increased (P<0.05); in the substantia nigra of midbrain, the number of positive cells of TH was increased (P<0.01), the number of co-expression positive cells of Notch1/Iba-1 was decreased (P<0.001), the protein expression of α-syn, Notch1, Hes1, Iba-1, iNOS, TNF-α, IL-6 and IL-1β was decreased (P<0.05, P<0.01), the protein expression of TH, ARG1 and IL-10 was increased (P<0.05, P<0.001, P<0.01), the mRNA expression of Notch1 and Hes1 was decreased (P<0.05). CONCLUSION EA can improve the behavioral performance and protect the dopaminergic neurons in PD mice, its mechanism may relate to the inhibition of Notch1/Hes1-mediated neuroinflammation, thus inhibiting the microglial activation.
Animals ; Electroacupuncture ; Microglia/metabolism* ; Male ; Receptor, Notch1/metabolism* ; Parkinson Disease/physiopathology* ; Transcription Factor HES-1/metabolism* ; Mice ; Mice, Inbred C57BL ; Humans ; Signal Transduction

OBJECTIVE: To analysis the medication characteristics of the prescriptions issued via open channel by the National and Provincial Health Committee and the State Administration of Traditional Chinese Medicine in treating coronavirus disease 2019 (COVID-19). METHODS: We collected the data of traditional Chinese medicine related to treatment plans published by the National and Provincial Health Committee and the State Administration of Traditional Chinese Medicine from the start of COVID-19 outbreak to February 19, 2020. The frequency analysis, cluster analysis and association analysis were performed. RESULTS: The study collected 4 national and 34 regional prevention and treatment plans, 578 items, 84 traditional Chinese formulations, 60 Chinese patent medicines, and 230 Chinese herbs. The high frequently used herbs were , and . The commonly used traditional formulations included decoction, powder, and decoction. The Chinese patent drugs included pill, injection, and capsule. The most common paired medications were and and Two core combinations and one novel formula were discovered in the study. CONCLUSIONS powder and decoction are the basic formulations for syndrome of COVID-19. In addition, decoction, powder, decoction and decoction are the basic formulations for syndrome of COVID-19. The main medication characteristics are clearing heat, entilating lung, removing toxicity and removing turbidity. It shows that removing toxicity and eliminating evil are the prescription thought in treating epidemic disease of traditional Chinese medicine.
Betacoronavirus ; isolation & purification ; Coronavirus Infections ; therapy ; Data Mining ; Drugs, Chinese Herbal ; chemistry ; therapeutic use ; Humans ; Medicine, Chinese Traditional ; Pandemics ; Pneumonia, Viral ; therapy

OBJECTIVE: To analysis the medication characteristics of the prescriptions issued via open channel by the National and Provincial Health Committee and the State Administration of Traditional Chinese Medicine in treating coronavirus disease 2019 (COVID-19). METHODS: We collected the data of traditional Chinese medicine related to treatment plans published by the National and Provincial Health Committee and the State Administration of Traditional Chinese Medicine from the start of COVID-19 outbreak in Wuhan to February 19, 2020. The frequency analysis, cluster analysis and correlation analysis were performed. RESULTS: The study collected 4 national and 34 regional prevention and treatment plans, 578 items, 84 traditional Chinese formulations, 60 Chinese patent medicines, and 230 Chinese herbs. The high frequently used herbs were , , , and . The commonly used traditional formulations included Decoction, Powder, and Decoction. The Chinese patent drugs included Pill, Injection, and Capsule. The most common paired medications were and , and . Two core combinations and one novel formula were discovered in the study. CONCLUSIONS Powder and Decoction are the basic formulations for syndrome of COVID-19. In addition, Decoction, Powder, Decoction and Decoction are the basic formulations for syndrome of COVID-19. The main medication characteristics are clearing heat, entilating lung, removing toxicity and removing turbidity. It shows that removing toxicity and eliminating evil are the prescription thought in treating epidemic disease of traditional Chinese medicine.
Betacoronavirus ; Cluster Analysis ; Coronavirus Infections ; therapy ; Data Mining ; Drugs, Chinese Herbal ; analysis ; therapeutic use ; Humans ; Medicine, Chinese Traditional ; statistics & numerical data ; Pandemics ; Pneumonia, Viral ; therapy