To study the changes in metabolites in platelets of a rat model of Qi deficiency and blood stasis syndrome using metabolomics methods and further elucidate the intervention effect of Buyang Huanwu Decoction（补阳还五汤，BYHWD）on Qi deficiency and blood stasis syndrome.

Thirty Sprague dawley（SD）rats were randomly divided into the normal，model and BYHWD groups. The model group established a sleep deprivation model through a multi-platform sleep deprivation system in the water environment. The BYHWD group was administered for two weeks after successful modeling，with sleep deprivation added simultaneously. The administration group was orally administered BYHWD at a clinical dose of 13 g· kg^-1，while the normal and model groups were orally administered an equal amount of distilled water once a day at the same time for 14 consecutive days. The construction of a comprehensive evaluation model and platelet function were evaluated from the perspectives of grip，coagulation function，platelet morphology，aggregation rate and CD62P（P-Selectin）expression rate. The metabolomics analysis of endogenous metabolites in rat platelets was carried out by using Ultra-high Performance Liquid Chromatography with Quadrupole Time-of-flight Mass Spectrometry（UPLC-Q-TOF-MS）. The detection conditions were reverse phase chromatography column（RPLC）and Hydrophilic Interaction Chromatography（HILIC）chromatographic column，mobile phase 0.1% formic acid aqueous solution（A）-0.1% formic acid acetonitrile solution（B）gradient elution，flow rate 0.3 mL· min^-1，electric spray ion source（ESI），positive and negative ion mode detection，scanning range m/z50-1000. The multivariate statistical analysis was used to screen the inter-group differential ions and match fragment ion information with databases such as the Human Metabolome Database（HMDB）to identify biomarkers. The biological information of metabolites was obtained through the Kyoto Encyclopedia of Genes and Genomes（KEGG）database，and their related metabolic pathways were analyzed using MetaboAnalyst 5.0 software.

Study showed that compared with that of the normal group，the grip of the model group decreased（P<0.01），and BYHWD significantly increased the grip compared to the model group（P<0.01）. Compared with that of the normal group，the activated partial thromboplastin time（APTT）of coagulation function in the model group decreased（P<0.01），while the thrombin time（TT）increased（P<0.05）and the level of fibrinogen（FIB）increased（P<0.05）. Compared with those of the model group，the APTT in the BYHWD group significantly increased（P<0.01），while FIB level decreased（P<0.05）. Compared with those of the normal group，the maximum platelet aggregation rate（MAR）and average platelet aggregation rate（AAR）of the model group rats were significantly increased（P<0.01）. Compared with those of the model group，the MAR and AAR of platelets in the BYHWD group were significantly reduced，with varying degrees of difference（P<0.01，P<0.05）. Compared with that of the normal group，the expression of platelet CD62Pin the model group was significantly increased（P<0.05），and the BYHWD group could significantly reduce the expression rate of platelet CD62P（P<0.05）. The scanning electron microscopy results showed that compared with the normal group，the model group showed excessive platelet activation，significant pseudopodia extension and increased aggregation between platelets. Compared with the model group，the BYHWD group had fewer platelet activation and aggregation phenomena. The metabolomics results showed that the platelet metabolism of the rat model with Qi deficiency and blood stasis syndrome was disrupted，resulting in 95 significantly different metabolites. The main differential metabolites were concentrated in fatty acids，amino acids，phosphatidylcholine，lysophosphatidylcholine，nucleotides，etc. The intervention effect of BYHWD on Qi deficiency and blood stasis syndrome was mainly reflected in the regulation of metabolic pathways such as lipid metabolism，amino acid metabolism，nucleic acid metabolism and energy metabolism.

Study preliminarily reveals the metabolomics characteristics of platelets in rats with Qi deficiency and blood stasis syndrome and provides a basis for the mechanism of action of BYHWD on platelets in the intervention of Qi deficiency and blood stasis syndrome.

Modern studies have shown that immune cells play an important role in the occurrence and development of ischemic stroke（IS）. Currently，the intrinsic mechanism of the theory of positive Qi-evil in traditional Chinese medicine（TCM）has not been elucidated yet，and a number of studies have suggested that immune cell-mediated immune homeostasis may be one of the important mechanisms of the theory of positive Qi-evil in TCM. In this paper，it used Mendelian randomization（MR）analysis to verify the causal relationship of immune cells on ISand further explored the intrinsic mechanism of the theory of positive Qi-evil.

Based on publicly available genetic data，a two-sample MR analysis was performed using immune cells as instrumental variables to explore the causal relationship between 731 immune cell phenotypes and the risk of IS prevalence. The inverse variance weighting（IVW）method as the primary method was used as a standardized analysis，supplemented by the use of weighted median，MR-Egger，Simple mode and Weighted mode. Cochrans Q was used to test the heterogeneity，and MR-Egger intercept to test the test-level pleiotropy.

Eleven immune cell phenotypes were still found to be statistically significant（P<0.05 corrected for FDR）：among them CD27 on memory B cell，CD27 on sw mem，CD27 on CD24^＋CD27^＋，CD27 on IgD^-CD38^dim，CD27 on IgD^-CD38^-，CD27 on IgD^-CD38^br，CD25 on IgD^＋and CD25 on IgD^＋CD38^dim play a dangerous role for IS；CD40 on CD14^-CD16^＋monocyte，CD40 on CD14^＋CD16^-monocyte and CD40 on CD14^＋CD16^＋monocyte play a protective role for IS. Eight of them were in the B-cell group and three in the monocyte group. It was significant with CD27 and CD25 on B cells and CD40 on monocytes.

This study confirmed that immune cells play a key role in ISby genetic means，providing some reference for elucidating the intrinsic mechanism of the theory of positive Qi-evil.

This study aimed to investigate the ameliorating effect of Qinjiao Wuwei Formula（秦艽五味方，QJF）on skin lesions in a mouse model of 2，4-dinitrofluorobenzene（DNFB）-induced atopic dermatitis（AD）-like mice and its mechanism.

The DNFB-induced mouse AD-like model was established，and the mice were randomly divided into blank control，model（DNFB），positive control（dexamethasone，DXMS）and QJF groups. The severity of skin lesions was evaluated using the Scoring Atopic Dermatitis Index（SCORAD），and the histomorphological changes and epidermal thickness of the lesions were observed under light microscopy. The number of mast cells was detected by toluidine blue staining，the expression of filaggrin（FLG）in skin lesions was detected by immunohistochemistry，and the expression of serum IgE was detected by ELISA. The proportion of Th1/Th2 cells in the spleen and lymph nodes，the proportion of Th17 cells in lymph nodes were tested by flow cytometry，and the differential expressions of inflammatory factors in serum were detected by high-throughput liquid-phase protein chip technology.

Compared with the model group，the QJFgroup had significantly reduced SCORAD scores and scratching index，thinner skin lesions，and a significant decrease in the number of mast cells in the lesions. The positive expression of FLG was restored，and the expression of IgE was reduced. The ratio of Th1/Th2 in the spleen and lymph nodes increased，while the proportion of Th17 cells in the lymph nodes was decreased. Furthermore，inflammatory cytokines in serum were all decreased after treatment with QJF，with the most significant regulatory effect on the expressions of Th2-related cytokines.

QJF can effectively improve the skin lesions of DNFB-induced AD-like mice while regulating the inflammatory response of Th2-related cytokines.

To observe the mechanism of electroacupuncture intervention on the activation of astrocytes in the hippocampal region of rats with cerebral ischemia-reperfusion injury and its effects on the expressions of reactive oxygen species（ROS），thioredoxin interacting protein（TXNIP）and nucleotidebinding oligomerization domain（NOD）-like receptor family pyrin domain containing 3（NLRP3）.

Forty-eight adult male SD rats were randomly divided into sham surgery group，model group，ROSinhibitor group and electroacupuncture group，with 12 rats in each group. The cerebral ischemia-reperfusion injury rat model was prepared using the traditional Koizumi suture method，and the rats were included or excluded according to the Longa scoring method. The sham surgery group only underwent the separation of the carotid artery. The inhibitor group received intragastric administration of the ROSinhibitor N-acetyl-L-cysteine solution for 10 days starting 3 days before modeling. The electroacupuncture group received intervention at Baihui（DU20），Yintang（DU29）and bilateral Zusanli（ST36）for 10 min per day for 7 days. Cylinder experiment was conducted to observe the recovery ofneurological function.TTC was used to detect the infarct area of the brain. The immunohistochemistry method was performed to detect the positive expression of GFAPin the hippocampal region.DHE fluorescence probe was used to detect ROScontent in the hippocampal region. Western blot was performed to detect the protein expressions of GFAP，TXNIP and NLRP3 in the hippocampal region，and immunofluorescence was used to determine the colocalization of TXNIPand NLRP3 in the hippocampal region.

Compared with the sham surgery group，the model group showed a significantly reduced asymmetry index，more severe neurological function damage（P<0.01），larger range of cerebral infarction area（P<0.01），increased expression and protein content of GFAP（P<0.01），less proliferation of astrocytes，weaker fiber protrusions of cell bodies，and significant increase in ROS，TXNIPand NLRP3（P<0.01）. Compared with the model group，the ROSinhibitor group and the electroacupuncture group showed higher asymmetry index，better recovery of neurological function（P<0.05，P<0.01），smaller range of cerebral infarction area（P<0.01），significantly increased expression and protein content of GFAP（P<0.01），increased activation of astrocyte proliferation，denser arrangement，increased degree of cell fiber protrusions，and decrease in the contents of ROS，TX-NIP and NLRP3（P<0.05，P<0.01），with the electroacupuncture group showing more significant effects than the inhibitor group.

Electroacupuncture intervention can restore neurological function damage in rats，which may be related to promoting the proliferation and activation of astrocytes，inhibiting the ROSTXNIP-NLRP3 signaling pathway，reducing oxidative stress and inflammatory reactions and exerting neuroprotective effects.