In Vitro and in Vivo Anticancer Activity of Pardaxin against Proliferation and Growth of Oral Squamous Cell Carcinoma

Pardaxin (H-GFFALIPKIISSPLFKTLLSAVGSALSSSGGQE-OH), a 33-amino-acid polypeptide, is an antimicrobial peptide (AMP) isolated from the marine fish species Pardachirus marmoratus. Pardaxin shows antibacterial and antitumor activities. However, pardaxin-induced inhibition of oral cancer and the mechanism of tumor reduction in buccal pouch carcinogenesis after pardaxin painting remain undetermined. Additionally, the toxic effects of pardaxin on normal tissue remain unclear. The present study investigated the anticancer activity of pardaxin in oral squamous cell carcinoma (OSCC) cells in the hamster buccal pouch model with or without 7,12-dimethylbenz[a]anthracene (DMBA) pretreatment. This is the first study to confirm the effects of pardaxin on normal tissue and its nontoxic effects in vivo. Cell viability assays and colony formation tests in OSCC cell lines (SCC-4) demonstrated that pardaxin reduced cell viability in a dose-dependent manner. Immunofluorescence staining of cleaved caspase-3 in SCC-4 cells revealed that expression of activated caspase-3 in SCC-4 cells significantly increased after 24-h treatment with pardaxin. Additionally, a cell cycle analysis indicated that pardaxin treatment resulted in the cell cycle arrest of SCC-4 cells in the G2/M phase, thereby limiting cell proliferation. Furthermore, pardaxin treatment substantially alleviated carcinogenesis in the DMBA-induced hamster buccal pouch model by lowering prostaglandin E₂ levels. These results suggest that pardaxin is a potential marine drug for adjuvant chemotherapy for human OSCC and oral cancer.     

蜜环菌多糖对损伤性胰岛细胞分泌功能的影响

培养大鼠胰岛素瘤细胞(INS-1),以四氧嘧啶(AXN)损伤细胞,培养液中加入不同浓度的多糖AMP-1,检测不同浓度AMP-1对INS-1细胞葡萄糖刺激的胰岛素和C肽分泌量的影响,同时检测细胞存活率。结果表明,一定浓度范围AMP-1对AXN损伤的INS-1细胞分泌胰岛素和C肽均具有一定的促进作用,尤其是在葡萄糖刺激浓度为16.7mmol·L-1时,效果显著;AMP-1可减少AXN对INS-1细胞的损伤,使INS-1细胞存活率增加。     

Effect and mechanism of Qing-Kai-Ling on endotoxin-induced fever in rabbits

AIM:To explore the antipyretic mechanism of Qing Kai-Ling (QKL) injection on endotoxin (ET)-induced fever in rabbits.METHODS:Rabbit models of endotoxin (ET)-induced fever were duplicated. The rectal temperature was measured by digital thermograph. The cAMP and IL-1β content in the hypothalamus (HP), the cAMP content in the cerebrospinal fluid (CSF), and the arginine vasopressin (AVP) content in the ventral septal area (VSA) were determined by radioimmunoassay.RESULTS:① QKL had significant antipyretic effect on ET-induced fever(P<0.01), ② The production of IL-1β and cAMP in HP was significantly inhibited by QKL treatment (P<0.01), ③ QKL markedly decreased the cAMP content in the CSF and AVP content in the VSA(P<0.01).CONCLUSION:The antipyretic mechanisms of QKL are probably due to inhibiting the production of the endogenous pyrogen and central mediator of fever, and meanwhile stimulating the release of the antipyretic substances.     

外源环腺苷酸对水稻纹枯病菌生长的影响研究初报

初步探讨了外源环腺苷酸(cAMP)对水稻纹枯病菌(Rhizoctonia solaniAG-1 IA)生长的影响。研究结果显示,外源cAMP能显著抑制该病原菌的径向生长,在终浓度达到10 mmoL/L时产生的强烈抑制作用还导致了菌丝的扭曲和产生大量非正常分枝,菌核形成的时间也被推迟。该结果证明了水稻纹枯病菌菌丝生长对外源cAMP的敏感性。这为进一步研究该病原菌相关的生长因子提供了有用的参考。     

脂肪细胞膜免疫技术的研究进展

综述了脂肪细胞膜免疫的种类及其降低动物胴体脂肪的作用机理和效果,阐述了目前存在的问题,并展望了脂肪细胞膜免疫技术的应用前景。     

Effects of scoparone on dopamine release in PC12 cells

The effects of scoparone on dopamine release in PC12 cells were investigated. Scoparone at 50–200 µM increased dopamine release into the culture medium. However, the released levels of dopamine by scoparone were not altered in the absence of extracellular Ca²⁺ and by adenylyl cyclase inhibitor MDL-12,330A. Scoparone increased phosphorylation of PKA, CaMK II and synapsin I. Scoparone also enhanced K⁺-induced levels of dopamine release by CaMK II phosphorylation. These results suggest that scoparone increases dopamine release by synapsin I phosphorylation via activation of PKA and CaMK II, which are mediated by cyclic AMP levels and Ca²⁺ influx.     

几种离子对豇豆根瘤腺苷酸琥珀酸裂解酶活性和最适PH值的影响

在含１５％（ｖ／ｖ）甘油和ｐＨ８．０的１００ｍｍｏｌ／ＬＴｒｉｃｉｎｅ缓冲液中，当离子浓度＜１５０ｍｍｏｌ／Ｌ时，Ｋ＋和Ｎａ＋离子是豇豆根瘤腺苷酸琥珀酸裂解酶（ＡＳＡＬ）的激活剂，其最适浓度约为７５ｍｍｏｌ／Ｌ，可分别提高酶活性４０％和３５％。Ｍｇ２＋离子是ＡＳＡＬ的抑制剂，能拮抗Ｋ＋和Ｎａ＋离子的激活效应。ＨＰＯ二４离子可显著降低酶活性，抑制效应与ＨＰＯ二４离子浓度呈正相关。在含１５％（ｖ／ｖ）甘油和ｐＨ６．６～８．０的１００ｍｍｏｌ／Ｌ磷酸盐缓冲液中，ＡＳＡＬ的最适ｐＨ值约为７．４，而在含１５％（ｖ／ｖ）甘油和ｐＨ７．４～８．６的Ｔｒｉｃｉｎｅ缓冲液中，ＡＳＡＬ的最适ｐＨ值约为８．２。     

Adenylates in the soil microbial biomass at different temperatures

Five soils from temperate sites (Germany; 2 arable and 3 grassland) were incubated aerobically at 5, 10, 15, 20, 25, 35, and 40 °C for 8 days. Soils were analysed for soil microbial biomass C, biomass N, AMP, ADP, and ATP to determine whether the increase in the ATP-to-microbial biomass C ratio with increasing temperature was either due to an increase in the adenylate energy charge (AEC) or de novo synthesis of ATP, or both. Around 80% of the variance in microbial biomass C and biomass N was explained by differences in soil properties, only 7% by the temperature treatments. Averaging the data of all 5 soils for each incubation temperature, the microbial biomass C content decreased with increasing temperature from 15 to 40 °C continuously by 2.5 μg g⁻¹ soil °C⁻¹ after 8-days' incubation. However, this decrease was not accompanied by a similar decrease in microbial biomass N. The average microbial biomass C/N ratio was 6.8. Between 54 and 76% of the variance in AMP, ADP, ATP and the sum of adenylates was explained by differences in soil properties and between 14 (ADP) and 27% (ATP) by the temperature treatments. However, temperature effects on AMP and ADP were variable and inconsistent. In contrast, ATP and consequently also the sum of adenylates increased continuously from 5 to 30 °C followed by a decline to 40 °C. The AEC showed similarly a small, but significant increase with increasing temperature from 0.73 to 0.85 at 30 °C. Consequently, the majority of the variance, i.e. roughly 60% in AEC values, but also in ATP-to-microbial biomass C ratios was explained by the incubation temperature. The mean ATP-to-microbial biomass C ratio increased from 4.7 μmol g⁻¹ at 5 °C to a 2.5 fold maximum of 12.0 μmol g⁻¹ at 35 °C. This increase was linear with a rate of 0.26 μmol ATP g⁻¹ microbial biomass C °C⁻¹. The energy for the extra ATP produced during temperature increase is probably derived from an accelerated turnover of endocellular C reserves in the microbial biomass.