Acori Tatarinowii Rhizoma is the dried rhizome of Acorus tatarinowii in the family of Tennantiaceae, which has the efficacy of opening up the orifices and expelling phlegm, awakening the mind and wisdom, and resolving dampness and opening up the stomach. Modern studies have shown that volatile oil is the main active ingredient of Acori Tatarinowii Rhizoma, and α-asarone and β-asarone have been proved to be the active ingredients in the volatile oil of Acori Tatarinowii Rhizoma, with pharmacological effects such as anti-Alzheimer's disease, antiepileptic, anti-Parkinson's disease, antidepressant, anticerebral ischemia/reperfusion injury, anti-thrombosis, lipid-lowering, and antitumor. By summarising and outlining the pharmacological effects of α-asarone and β-asarone and elucidating the possible mechanisms of their pharmacological effects, we can provide theoretical basis for the further research and clinical application of Acori Tatarinowii Rhizoma.
Allylbenzene Derivatives ; Acorus/chemistry* ; Anisoles/chemistry* ; Rhizome/chemistry* ; Drugs, Chinese Herbal/chemistry* ; Humans ; Animals

OBJECTIVES: To investigate the regulatory role of astrocytes in the dorsomedial hypothalamus (DMH) during sevoflurane anesthesia emergence. METHODS: Forty-two male C57BL/6 mice were randomized into 6 groups (n=7) for assessing astrocyte activation in the dorsomedial hypothalamus (DMH) under sevoflurane anesthesia. Two groups of mice received microinjection of agfaABC1D promoter-driven AAV2 vector into the DMH for GCaMP6 overexpression, and the changes in astrocyte activity during sevoflurane or air inhalation were recorded using calcium imaging. For assessing optogenetic activation of astrocytes, another two groups of mice received microinjection of an optogenetic virus or a control vector into the DMH with optic fiber implantation, and sevoflurane anesthesia emergence was compared using behavioral experiments. In the remaining two groups, electroencephalogram (EEG) recording during sevoflurane anesthesia emergence was conducted after injection of the hChR2-expressing and control vectors. Anesthesia induction and recovery were assessed by observing the righting reflex. EEG data were recorded under 2.0% sevoflurane to calculate the burst suppression ratio (BSR) and under 1.5% sevoflurane for power spectrum analysis. Immunofluorescence staining was performed to visualize the colocalization of GFAP-positive astrocytes with viral protein signals. RESULTS: Astrocyte activity in the DMH decreased progressively as sevoflurane concentration increased. During 2.0% sevoflurane anesthesia, the mice injected with the ChR2-expressing virus exhibited a significantly shortened wake-up time (P<0.05), and optogenetic activation of the DMH astrocytes led to a marked reduction in BSR (P<0.001). Under 1.5% sevoflurane anesthesia, optogenetic activation resulted in a significant increase in EEG gamma power and a significant decrease in delta power in ChR2 group (P<0.01). CONCLUSIONS Optogenetic activation of DMH astrocytes facilitates sevoflurane anesthesia emergence but does not significantly influence anesthesia induction. These findings offer new insights into the mechanisms underlying anesthesia emergence and may provide a potential target for accelerating postoperative recovery and managing anesthesia-related complications.
Animals ; Astrocytes/physiology* ; Sevoflurane ; Mice, Inbred C57BL ; Mice ; Male ; Electroencephalography ; Anesthetics, Inhalation/pharmacology* ; Hypothalamus/cytology* ; Anesthesia Recovery Period ; Methyl Ethers/pharmacology*

Sevoflurane is one of the most commonly used inhaled anesthetics in obstetric and pediatric general anesthesia.According to related literature,this article reviews major possible mechanisms including myelin formation damage,nerve inflammation,cell apoptosis,oxidative stress,inhibition of histone acetylation,synapsis and receptor changes of sevoflurane-induced neurotoxicity in animal experiments.Furthermore,we summarize the neuroprotection effects and functioning mechanisms of anti-anemia medicine,plant-based drugs,alpha 2 adrenoceptor agonists and others,aiming to provide a basis for the brain protection of fetuses and infants during the perioperative period.
Anesthetics, Inhalation/adverse effects* ; Animals ; Apoptosis ; Brain ; Child ; Female ; Humans ; Methyl Ethers ; Neuroprotective Agents/therapeutic use* ; Oxidative Stress ; Pregnancy ; Sevoflurane

To investigate effects of α-asarone and β-asarone on induced PC12 cell injury and related mechanisms. Aβ toxic injury cell model was induced by Aβ in PC12 cells. PC12 cells were divided into blank control group, model control group, α-asarone group (0.5, 1.0, β-asarone group (6.3, 12.5, vasoactive intestinal peptide (VIP) group, and VIP antagonist control group. Cell survival rate was detected by CCK-8 kit; cell apoptosis rate was detected by flow cytometry. The levels of inflammatory cytokines interleukin (IL)-1, , tumor necrosis factor (TNF)-α, oxidation-related inducible nitric oxide synthase (iNOS), nitric oxide (NO), apoptosis factors caspase-3 and p53 were detected by ELISA method. The expressions of C-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (p38MAPK) were detected by Western blotting. Compared with model control group, cell survival rates of group, β-asarone group and VIP group increased; the cell apoptosis rate decreased; levels of apoptosis-related factors caspase-3, p53, inflammatory factors IL-1, TNF-α decreased; IL-10 level increased; levels of oxidization-related factors iNOS and NO decreased; the expression of JNK and p38MAPK protein decreased (all <0.05). After VIP antagonist intervention, the survival rate of β-asarone group decreased; apoptosis rate increased; apoptosis related factors caspase-3, p53, inflammatory factors IL-1, TNF-α increased; IL-10 decreased; oxidation related factors iNOS and NO increased; the expression of JNK and p38MAPK protein increased (all <0.05); while there were no significant changes in these indicators of α-asarone group (all >0.05). α-asarone and β-asarone have protective effects on PC12 cell injury induced by Aβ. β-asarone may inhibit inflammatory factors and oxidation-related factors through promoting VIP secretion, regulating JNK/MAPK pathway, and reducing PC12 cell apoptosis; however, the effect of α-asarone may be not related to VIP secretion.
Allylbenzene Derivatives ; Animals ; Anisoles/pharmacology* ; Apoptosis ; PC12 Cells ; Rats

To prepare and optimize the self-microemulsion co-loaded with tenuifolin and β-asarone(TF/ASA-SMEDDS) and evaluate its quality. The prescription compositions of TF/ASA-SMEDDS were screened by solubility test, single factor test and pseudo-tern-ary phase diagram, and the prescriptions were further optimized by Box-Behnken response surface method, with the drug loading and particle size as the evaluation indexes. Then the optimized TF/ASA-SMEDDS was evaluated for emulsified appearance, particle size, morphology and drug release in vitro. The optimized prescription for TF/ASA-SMEDDS was as follows: caprylic citrate triglyceride polyoxyethylene castor oil-glycerol(10.8∶39.2∶50), drug loading of(5.563±0.065) mg·g~(-1) for tenuifolin and(5.526±0.022) mg·g~(-1) for β-asarone; uniform and transparent pan-blue nanoemulsion can be formed after emulsification, with particle size of(28.84±0.44) nm. TEM showed that TF/ASA-SMEDDS can form spherical droplets with a uniform particle size after emulsification; In vitro release test results showed that the drug release rate and cumulative release of tenuifolin and β-asarone were significantly improved. The preparation process of TF/ASA-SMEDDS was simple and can effectively improve in vitro release of tenuifolin and β-asarone.
Anisoles ; Biological Availability ; Diterpenes, Kaurane ; Drug Delivery Systems ; Emulsions ; Particle Size ; Solubility ; Surface-Active Agents

OBJECTIVE: To study the protective effect of isoflurane preconditioning on hepatic ischemia-reperfusion (I/R) injury mediated by the noncanonical pyroptosis pathway. METHODS: Thirty C57BL/6 mice were randomly divided into sham-operated group, isoflurane group and I/R group, and in the latter two groups, hepatic I/R injury was induced by clamping the portal vein for 30 min. In isoflurane group, the mice were pretreated with 1.4% isoflurane 30 min before the surgery. The protective effect of isoflurane preconditioning against hepatic I/R injury was evaluated by assessing the pathological score of HE staining of the liver tissue and serum ALT and AST levels. Serum IL-1β and IL-18 levels and the protein expression of GSDMS were detected by ELISA and Western blotting to evaluate the inhibitory effect of isoflurane preconditioning on pyroptosis. Western blotting and immunofluroescence were used to detect the protein expression of caspase-11 in the liver tissues to evaluate the inhibitory effect of isoflurane preconditioning on noncanonical pyroptosis pathway. RESULTS: The Suzuki's score of the liver tissue was significantly higher in I/R group than in the sham group ( < 0.05), while the score in the isoflurane group was significantly lower than that in the I/R group ( < 0.05). Serum ALT and AST levels significantly increased in the sham group ( < 0.05), and were significantly lower in isoflurane group than in I/R group ( < 0.05). The serum levels of IL-1β and IL-18 were significantly higher in I/R group than in sham group ( < 0.05), and were significantly lower in isoflurane group than in I/R group ( < 0.05). The expression of GSDMD in the I/R group was significantly higher than that in sham group, and was significantly lower in isoflurane group than in I/R group ( < 0.05). The hepatic expression of caspase-11 was significantly higher in I/R group than in sham group ( < 0.05), and was significantly lower in isoflurane group than in I/R group ( < 0.05). CONCLUSIONS Isoflurane preconditioning has protective effect against hepatic I/R injury, which is related to the inhibition of the noncanonical pyroptosis pathway.
Animals ; Caspases, Initiator ; Ischemic Preconditioning ; Isoflurane ; Liver ; Mice ; Mice, Inbred C57BL ; Pyroptosis ; Reperfusion Injury

BACKGROUND: Resting-state functional magnetic resonance imaging (rs-fMRI) is a promising method for the study of brain function. Typically, rs-fMRI is performed on anesthetized animals. Although different functional connectivity (FC) in various anesthetics on whole brain have been studied, few studies have focused on different FC in the aged brain. Here, we measured FC under three commonly used anesthesia methods and analyzed data to determine if the FC in whole brain analysis were similar among groups. METHODS: Twenty-four male aged Wistar rats were randomly divided into three groups (n = 8 in each group). Anesthesia was performed under either isoflurane (ISO), combined ISO + dexmedetomidine (DEX) or α-chloralose (AC) according to the groups. Data of rs-fMRI was analyzed by FC in a voxel-wise way. Differences in the FC maps between the groups were analyzed by one-way analysis of variance and post hoc two-sample t tests. RESULTS: Compared with ISO + DEX anesthesia, ISO anesthesia caused increased FC in posterior brain and decreased FC in the middle brain of the aged rat. AC anesthesia caused global suppression as no increase in FC was observed. CONCLUSION ISO could be used as a substitute for ISO + DEX in rat default mode network studies if the left temporal association cortex is not considered important.
Anesthesia ; Animals ; Brain/diagnostic imaging* ; Brain Mapping ; Isoflurane ; Magnetic Resonance Imaging ; Male ; Rats ; Rats, Wistar

Objective To study the influence of halogenated hydroxyl-alkanes inhalation anesthetic on the determination of ethanol content in blood. Methods Halogenated hydroxyl-alkanes were analyzed by headspace gas chromatography with double column confirmatory detection method. The influence of halogenated hydroxyl-alkanes on determination of ethanol content in blood sample by headspace gas chromatography was explored under the different detection conditions of KB-BAC1/ KB-BAC2 and J&W DB-ALC1/DB-ALC2 gas chromatographic column. Results The retention time of sevoflurane and enflurane was similar to that of ethanol and tert butanol respectively when using the J&W DB-ALC1/DB-ALC2 gas chromatographic column, and interfered with the detection of ethanol content in blood; only J&W DB-ALC1 gas chromatographic column can separate the sevoflurane and ethanol components, so as to eliminate their influence on the detection of ethanol content in blood. When using KB-BAC1/KB-BAC2 gas chromatographic column, the retention time of sevoflurane, isoflurane and ethanol is similar, especially that of sevoflurane and ethanol, and sevoflurane obviously interferes with the determination of ethanol content in blood. Conclusion Halogenated hydroxy-alkanes interfere with determination of ethanol content in blood by headspace gas chromatography. The interference can be discriminated effectively by choosing the suitable chromatographic column and double column confirmatory detection.
Alkanes ; Anesthetics, Inhalation ; Ethanol ; Isoflurane ; Sevoflurane

OBJECTIVE: To investigate the effect of ulinastatin pretreatment on isoflurane-induced mitochondria-dependent neuronal apoptosis in the hippocampus of rats. METHODS: Thirty-six male SD rats were randomly assigned into control group, isoflurane group and ulinastatin group. In the latter two groups, the rats were subjected to acute exposure to 0.75% isoflurane for 6 h and pretreated with 50 000 U/kg of ulinastatin before isoflurane exposure, respectively. After the treatments, apoptosis of the hippocampal neurons was detected using TUNEL assay, and the mitochondrial membrane potential (△ ψm) was measured using JC-1 mitochondrial membrane potential kit; cytochrome C release and caspase-3 activity were examined with Western blotting, and intracellular reactive oxygen species (ROS) was detected using the fluorescent probe H2DCFDA. RESULTS: Compared with those in the control group, the rats with acute exposure to isoflurane showed markedly increased TUNEL-positive cells in the hippocampus ( < 0.05), which were obviously reduced by ulinastatin pretreatment ( < 0.05). The △ψm of the hippocampal neurons was significantly reduced after isoflurane exposure ( < 0.05), and was partly recovered by ulinastatin pretreatment ( < 0.05). Acute exposure to isoflurane resulted in obviously increased cellular ROS, cytochrome C release and caspase-3 activity in the hippocampal neurons ( < 0.05), and these changes were significantly inhibited by ulinastatin pretreatment ( < 0.05). CONCLUSIONS Ulinastatin pretreatment provides neuroprotection against isoflurane-induced apoptosis of the hippocampal neurons in rats possibly by inhibiting mitochondria-dependent apoptosis pathway.
Animals ; Apoptosis ; Glycoproteins ; Hippocampus ; Isoflurane ; Male ; Rats ; Rats, Sprague-Dawley

STUDY DESIGN: Prospective, randomized, double blind, placebo-controlled study.PURPOSE: To compare clonidine and pregabalin with placebo for the attenuation of postoperative pain after thoracolumbar spinal surgery and instrumentationOVERVIEW OF LITERATURE: Spine surgery is associated with moderate to severe postoperative pain that needs to be controlled to improve patient’s outcome. Alpha 2 agonists (e.g., clonidine) and gabapentenoids (e.g., pregabalin) are successfully used as part of a multimodal analgesic regimen.METHODS: Total 75 patients were enrolled and randomly allocated into three groups. Group P received pregabalin (150 mg), group C received clonidine (150 mcg), and group N received placebo 90 minutes preoperatively. A standard anesthesia protocol comprising fentanyl, thiopentone, vecuronium, nitrous oxide, and oxygen in isoflurane was used for all patients. Postoperative recovery profile, pain, time for first analgesic, 24-hour analgesic requirement, sedation, and hemodynamic parameters were noted.RESULTS: Recovery profile was similar in all three groups; however, the patients in group P and C were more sedated (p<0.05). Group N patients had a higher Visual Analog Scale (VAS) score (p<0.05) and the time for first analgesic was also lower (p=0.02). Postoperative (24-hour) analgesic requirement was maximum in group N, followed by that in group C and group P. The VAS score was highest in the control group; however, after 12 hours, it was similar in all groups.CONCLUSIONS: Postoperative pain and analgesic requirement is significantly attenuated by preoperative administration of a single dose of clonidine (150 mcg) or pregabalin (150 mg); pregabalin was more effective. Thus, their use offers a reasonable strategy for pain management in patients undergoing spine surgery.
Analgesics ; Anesthesia ; Clonidine ; Fentanyl ; Hemodynamics ; Humans ; Isoflurane ; Nitrous Oxide ; Oxygen ; Pain Management ; Pain, Postoperative ; Pregabalin ; Prospective Studies ; Spine ; Thiopental ; Vecuronium Bromide ; Visual Analog Scale