ObjectiveTo investigate the effects of paeoniflorin （PF） on neuroinflammation and cognitive impairment in the rat model of Alzheimer's disease （AD） and to clarify whether its mechanism is associated with regulation of the Janus kinase 2 （JAK2）/signal transducer and activator of transcription 3 （STAT3） signaling pathway. MethodsGlycosides related to AD-associated neuroinflammation were screened through bibliometric analysis， and the potential targets of PF were predicted through network pharmacology and molecular docking. A rat model of AD was established by intraperitoneal injection of D-galactose （100 mg·kg^-1·d^-1）. Rats were assigned into a control group， a model group， a PF （200 mg·kg^-1） group， and a donepezil （0.5 mg·kg^-1·d^-1） group， and drugs were administered by gavage for 21 days. The learning and memory abilities were evaluated by the Morris water maze （MWM）. Hematoxylin-eosin （HE） staining and Nissl staining were performed to observe hippocampal neuronal morphology. The mRNA levels of inflammatory factors were determined by Real-time quantitative polymerase chain reaction （Real-time PCR）， and the protein levels of molecules in the JAK2/STAT3 signaling pathway were determined by Western blot. ResultsCompared with the control group， the model group showed prolonged escape latency and decreased platform crossings and time spent in the target quadrant （P<0.05， P<0.01）， accompanied by increased expression of interleukin-1β （IL-1β） and tumor necrosis factor-α （TNF-α）， as well as elevated ratios of phosphorylated （p）-JAK2/JAK2 and p-STAT3/STAT3 （P<0.01）. Compared with the model group， the PF group and donepezil group exhibited shortened escape latency and increased platform crossings and time spent in the target quadrant （P<0.05， P<0.01）， decreased expression levels of IL-1β and TNF-α， upregulated mRNA levels of interleukin-4 （IL-4） and interleukin-10 （IL-10）， and reduced ratios of p-JAK2/JAK2 and p-STAT3/STAT3 （P<0.05， P<0.01）. ConclusionPaeoniflorin can alleviate cognitive impairment and neuroinflammation in the rat model of AD by inhibiting the JAK2/STAT3 signaling pathway.

A 45-year-old man with about 10 years of drug abuse history took 96 tablets of sodium valproate sustained-release ( 48 g ) and about 20 capsules of ziprasidone hydrochloride (>400 mg ) by himself one time. He appeared comatous and had no response to being called, then he was sent to the hospital by his family members. He presented no autonomous respiration, hypotonia of the four limbs and neck (2 level) on admission. He received symptomatic supportive treatments including tracheal intubation and ventilator assisted breathing, gastric lavage, coloclyster, fluid infusion, diuresis, and central nervous system stimulant, immediately. Two hours later, the patient awoke. Laboratory tests revealed the following results:arterial oxygen partial pressure (PaO2) 292 mmHg (1 mmHg=0. 133 kPa), lactic acid 5. 70 mmol/L, D-dimer 7. 8 mg/L, plasma fibrinogen degradation product (FDP) 45 mg/L. Twenty-four hours later, laboratory tests revealed the following results:PaO298 mmHg, lactic acid 1. 7 mmol/L, D-dimer 2. 2 mg/L, FDP 19 mg/L. The trachea cannula was removed. Forty-eight hours later, his consciousness returned to normal. He could finish the common action. But he still had the symptom of drowsiness. Seven days later, the patient could answer questions accurately. His muscular tension returned to normal. He had light drowsiness occasionally.

A 45-year-old man with about 10 years of drug abuse history took 96 tablets of sodium valproate sustained-release ( 48 g ) and about 20 capsules of ziprasidone hydrochloride (>400 mg ) by himself one time. He appeared comatous and had no response to being called, then he was sent to the hospital by his family members. He presented no autonomous respiration, hypotonia of the four limbs and neck (2 level) on admission. He received symptomatic supportive treatments including tracheal intubation and ventilator assisted breathing, gastric lavage, coloclyster, fluid infusion, diuresis, and central nervous system stimulant, immediately. Two hours later, the patient awoke. Laboratory tests revealed the following results:arterial oxygen partial pressure (PaO2) 292 mmHg (1 mmHg=0. 133 kPa), lactic acid 5. 70 mmol/L, D-dimer 7. 8 mg/L, plasma fibrinogen degradation product (FDP) 45 mg/L. Twenty-four hours later, laboratory tests revealed the following results:PaO298 mmHg, lactic acid 1. 7 mmol/L, D-dimer 2. 2 mg/L, FDP 19 mg/L. The trachea cannula was removed. Forty-eight hours later, his consciousness returned to normal. He could finish the common action. But he still had the symptom of drowsiness. Seven days later, the patient could answer questions accurately. His muscular tension returned to normal. He had light drowsiness occasionally.