Effects and mechanisms of tanshinone IIA on PTSD-like symptoms.

BACKGROUND: In recent years, Salvia miltiorrhiza and its active substances have remarkably progressed in treating central neurological disorders. Tanshinone IIA (TSA) is an active ingredient derived from the rhizome of Salvia miltiorrhiza that has been found to alleviate the symptoms of several psychiatric illnesses. Post-traumatic stress disorder (PTSD) is a mental disorder that results after experiencing a serious physical or psychological injury. The currently used drugs are not satisfactory for the treatment of PTSD. However, it has been reported that TSA can improve PTSD-like symptoms like learning and memory, cognitive disorder, and depression through multi-target regulation. PURPOSE: This paper discusses the ameliorative effects of TSA on PTSD-like symptoms and the possible mechanisms of action in terms of inhibition of neuronal apoptosis, anti-neuroinflammation, and anti-oxidative stress. Based on the pathological changes and clinical observations of PTSD, we hope to provide some reference for the clinical transformation of Chinese medicine in treating PTSD. METHODS: A large number of literatures on tanshinone in the treatment of neurological diseases and PTSD were retrieved from online electronic PubMed and Web of Science databases. CONCLUSION: TSA is a widely studied natural active ingredient against mental illness. This review will contribute to the future development of TSA as a new clinical candidate drug for improving PTSD-like symptoms.

[Effect of electroacupuncture on degradation of myosin heavy chain of gastrocnemius muscle in diabetes rats].

OBJECTIVE: To explore the effect of electroacupuncture（EA）on the expression of muscle-specific ring finger protein 1（MuRF1/Trim63），F-box only protein 32（Fbxo32），myosin heavy chain-IIa（Myh2），myosin heavy chain-IIb（Myh4）and myosin heavy chain-I（Myh7）in diabetes rats. METHODS: Thirty-six male Wistar rats were equally randomized into control, model and EA groups. The diabetes model was established by intraperitoneal injection of 0.1% Streptozocin (STZ) solution (50 mg/kg). After that, EA (2 Hz, 1 mA) was applied to bilateral "Zusanli" (ST36), "Yinlingquan" (SP9) and "Shenshu" (BL23) for 10 min, once a day, 6 times a week for 2 weeks. The fasting blood glucose (FBG) and fasting serum insulin (FINS) contents were assayed by using ELISA, and the homeostasis model assessment of insulin resistance (HOMA-IR) was calculated. The body weight, and wet weight of bilateral gastrocnemius muscles were measured. The cross-sectional area (CSA) of the gastrocnemius muscle was measured after H.E. stai-ning. The expression of MuRF1, Fbxo32, Myh2, Myh4 and Myh7 mRNAs in the gastrocnemius tissue was tested using quantitative real time-PCR. RESULTS: Compared with the control group, the FBG and HOMA-IR were significantly higher (P<0.05), and the FINS, body weight were significantly lower (P<0.05) after intravenous injection of STZ for 1, 2, 3, 4, 5 weeks respectively. Following EA treatment and compared with the model group, the FBG and HOMA-IR were significantly down-regulated (P<0.05), and the FINS and body weight were considerably increased (P<0.05). Following modeling and compared with the control group, the wet weight of gastrocnemius muscle, CSA, and expression levels of Myh2, Myh4 and Myh7 mRNAs were obviously decreased, and the expression of MuRF1 and Fbxo32 mRNA was obviously increased in the model group (P<0.05). After EA treatment, the gastrocnemius muscle wet weight, CSA, expression levels of Myh2, Myh4 and Myh7 mRNA were significantly up-regulated (P<0.05), and the expression levels of MuRF1 and Fbxo32 mRNA were markedly down-regulated in comparison with those of the model group (P<0.05). CONCLUSION: EA treatment can delay the atrophy of gastrocnemius muscle (skeletal muscle) in diabetes rats possibly by improving the degradation of myosin heavy chain via regulating the expression of muscular MuRF1, Fbxo32, Myh2, Myh4 and Myh7 mRNAs.

High-dose glucocorticoids induce decreases calcium in hypothalamus neurons via plasma membrane Ca(2+) pumps.

In our previous studies, we occasionally found that high-dose glucocorticoids (GC) induced decrease in [Ca(2+)](i) in hypothalamus neurons. In previous articles, modulation of Ca(2+) channels by GC has been shown to contribute to the elementary regulation of several neuronal functions. However, little is known about the regulation of the Ca efflux pathways that counterbalance the Ca(2+) influx in neurons caused by high-dose GC. In this study, we demonstrate that a high-dose of GC (10 M dexamethasone) caused a 20% decrease in [Ca(2+)](i) within 2 s in cultured hypothalamic neurons; furthermore, we show that an antagonist of the GC receptor blocks this action. To ascertain the temporal sequence of relevant calcium transport mechanisms we selectively blocked the main calcium transporters, including sodium/calcium exchanger (NCX), plasma membrane calcium pumps (PMCA), and P-type Ca(2+)-ATPases of the sarcoplasmic reticulum (SERCA). The GC-induced [Ca(2+)](i) decrease disappeared completely when PMCA was blocked, but not when NCX and SERCA were blocked. These results suggest that high-dose GC (10(-6) M) rapidly decreases [Ca(2+)](i) by activating PMCA but not NCX or SERCA.