Acorus tatarinowii Schott: A Review of Its Botany, Traditional Uses, Phytochemistry, and Pharmacology.

Acorus tatarinowii Schott (A. tatarinowii) is a natural medicinal plant. It plays an indispensable role in the treatment of diseases by the empirical medicine system and has achieved remarkable curative effects. A. tatarinowii is often used to treat various diseases, such as depression, epilepsy, fever, dizziness, heartache, stomachache, etc. More than 160 compounds of different structural types have been identified in A. tatarinowii, including phenylpropanoids, terpenoids, lignans, flavonoids, alkaloids, amides, and organic acids. These bioactive ingredients make A. tatarinowii remarkable for its pharmacological effects, including antidepressant, antiepileptic, anticonvulsant, antianxiety, neuroprotective, antifatigue, and antifungal effects, improving Alzheimer's disease, and so on. It is noteworthy that A. tatarinowii has been widely used in the treatment of brain diseases and nervous system diseases and has achieved satisfactory therapeutic effects. This review focused on the research publications of A. tatarinowii and aimed to summarize the advances in the botany, traditional uses, phytochemistry, and pharmacology, which will provide a reference for further studies and applications of A. tatarinowii.

A Neural Circuit from the Paraventricular Thalamus to the Bed Nucleus of the Stria Terminalis for the Regulation of States of Consciousness during Sevoflurane Anesthesia in Mice.

BACKGROUND: The neural circuitry underlying sevoflurane-induced modulation of consciousness is poorly understood. This study hypothesized that the paraventricular thalamus bed nucleus of the stria terminalis pathway plays an important role in regulating states of consciousness during sevoflurane anesthesia. METHODS: Rabies virus-based transsynaptic tracing techniques were employed to reveal the neural pathway from the paraventricular thalamus to the bed nucleus of the stria terminalis. This study investigated the role of this pathway in sevoflurane anesthesia induction, maintenance, and emergence using chemogenetic and optogenetic methods combined with cortical electroencephalogram recordings. Both male and female mice were used in this study. RESULTS: Both γ-aminobutyric acid-mediated and glutamatergic neurons in the bed nucleus of the stria terminalis receive paraventricular thalamus glutamatergic projections. Chemogenetic inhibition of paraventricular thalamus glutamatergic neurons prolonged the sevoflurane anesthesia emergence time (mean ± SD, hM4D-clozapine N-oxide vs. mCherry-clozapine N-oxide, 281 ± 88 vs. 172 ± 48 s, P < 0.001, n = 24) and decreased the induction time (101 ± 32 vs. 136 ± 34 s, P = 0.002, n = 24), as well as the EC5 0 for the loss or recovery of the righting reflex under sevoflurane anesthesia (mean [95% CI] for the concentration at which 50% of the mice lost their righting reflex, 1.16 [1.12 to 1.20] vs. 1.49 [1.46 to 1.53] vol%, P < 0.001, n = 20; and for the concentration at which 50% of the mice recovered their righting reflex, 0.95 [0.86 to 1.03] vs. 1.34 [1.29 to 1.40] vol%, P < 0.001, n = 20). Similar results were observed during suppression of the paraventricular thalamus bed nucleus-stria terminalis pathway. Optogenetic activation of this pathway produced the opposite effects. Additionally, transient stimulation of this pathway efficiently induced behavioral arousal during continuous steady-state general anesthesia with sevoflurane and reduced the depth of anesthesia during sevoflurane-induced burst suppression. CONCLUSIONS: In mice, axonal projections from the paraventricular thalamic neurons to the bed nucleus of the stria terminalis contribute to regulating states of consciousness during sevoflurane anesthesia.

A study on the thyroid injury induced by combined deficiency of selenium,protein and vitamin E in rats / 中国地方病学杂志

Objective To explore the effect of associated deficiency of selenium,protein and vitamin E(VE)on the thyroid iniury and thyroid hormone metabolism of the rats in a long-term.Methods The Wistar rats were randomly divided into four groups:Group A with selenium deficiency and low protein and VE;Group B with selenium deficiency,low protein but adequate VE;Group C,adequate selenium and protein but low VE;Group D,adequate selenium.protein and VE.The rats were killed at the end of 26th week.Glutathione peroxidase(GSH-Px)activity in the rat blood and type I 5'-deiodinase activity of the rat liver were determined.The content of triiodothyronine(T3),tetraiodothyronine(T4),thyrotropic-stimulating hormone(TSH),activated oxygen(ROS)and malonaldehyde(MDA)were detected in serum. The changes of thyroid histopathology were observed under light microscope.Results ①The interactive effect of selenium+protein and VE was not significant on GSH-Px and ID I activity(F=0.003,0.871,P＞0.05),but it was significant on MDA and ROS content(F=13.057,6.706,P＜0.05 or＜0.01). ②Selenium+protein and VE could influence T3 and T4 content(F=431.977,28.271,6.570,41.419,P＜0.05).The interactive effect of selenium±protein and VE was not significant on T3 and T4 content(F=0.871,0.136,P＞0.05).Whether in the condition of low selenium and protein or supplementary,T4 contents of supplementary VE group[(79.095±12.199),(64.392±6.261)μg/L]were respectively higher than the low VE group[(61.068±6.648),(44.176±7.090)μg/L],the difference being statistically significant(t = 3.670,6.045, P ＜ 0.01). In the condition of low VE, T3[(0.718 ± 0.079)μg/L] and T4[(44.176 ±7.090)μg/L] content of supplementary selenium and protein group was lower than that in the low selenium and protein group[ (0.966 ± 0.156), (61.068 ± 6.648)μg/L], the difference being statistically significant (t = 4.568,4.916, P ＜0.01 ). With supplementary VE, T4 content of supplementary selenium and protein group[ (64.392 ± 6.261 )μg/L] was lower than that in the low selenium and protein group [(79.095 ± 12.199)μg/L], the difference being statistically significant (t = 3.033, P ＜ 0.01 ). ③Degeneration and necrosis of follicular epithelial cell were induced by diet of low selenium, protein and VE, which could be relieved by supplymentary VE. The sparseness of intracavitary glue was observed occationally in the supplementary selenium and protein but low VE group. Conclusions Long-term deficiency of selenium, protein and VE results in the decrease of the selenoenzymes of rats, which causes accumulation of the oxidative products, as well as thyroid pathological injury and thyroid hormone metabolism disorder, but supplement of adequate VE can reduce the oxidative damage in rats having low selenium and protein diet.