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目的 探讨和厚朴酚对脑出血（intracerebral hemorrhage，ICH）小鼠神经损伤和认知功能的影响及其作用机制。 方法 将C57BL/6J小鼠随机分为假手术组，模型组，和厚朴酚低、中、高剂量组，以及和厚朴酚+抑制剂组。除假手术组外，其余组小鼠均通过自体血注入右侧基底神经节构建ICH模型。于ICH前15 min和ICH后1 h，和厚朴酚低、中、高剂量组分别腹腔注射10 mg/kg、20 mg/kg、40 mg/kg和厚朴酚，和厚朴酚+抑制剂组腹腔注射40 mg/kg和厚朴酚与5 μg/kg脑源性神经营养因子（brain derived neurotrophic factor，BDNF）-酪氨酸激酶受体B（tyrosine kinase receptor B，TrkB）-环磷酸腺苷反应元件结合蛋白（cyclic adenosine monophosphate response element binding protein，CREB）信号通路抑制剂K252a，假手术组、模型组腹腔注射等量的二甲基亚砜和生理盐水。采用改良的神经功能缺损评分（modified neurological severity score，mNSS）评估小鼠神经功能；通过Morris水迷宫实验计算逃避潜伏期、跨越原平台次数、目标象限停留时间百分比3个指标用于评估小鼠空间学习和记忆能力；苏木精-伊红（hematoxylin-eosin，HE）染色观察海马神经元病理学改变；原位末端转移酶标记（terminal-deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling，TUNEL）染色检测海马神经元凋亡率；酶联免疫吸附试验（enzyme-linked immunosorbent assay，ELISA）检测血清BDNF、TrkB水平；免疫印迹法检测海马组织BDNF、TrkB、CREB、磷酸化CREB（phosphorylated CREB，p-CREB）蛋白表达情况。 结果 与假手术组小鼠相比，模型组小鼠mNSS、海马神经元凋亡率升高，逃避潜伏期延长，跨越原平台次数减少，目标象限停留时间百分比降低，血清BDNF、TrkB及海马组织BDNF、TrkB、p-CREB/CREB水平降低（均P

Copyright of Chinese Journal of Stroke is the property of Chinese Journal of Stroke Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The purpose of this study was to study the anti-inflammatory effects of magnolol and honokiol on intestinal injury induced by lipopolysaccharide in mice. A total of 135 healthy male ICR mice weighing 18~22 g were randomly divided into nine groups with three replicates in each group and five mice in each replicate. The groups were control group, model group, positive drug group (100 mg/kg berberine hydrochloride) and low, medium and high dose groups of magnolol and honokiol (25, 50, 100 mg/kg). Before modeling, mice were given gastric perfusion for seven days according to the test group, while the control group and model group were given gavage of normal saline. Inflammation was induced by intraperitoneal injection of 6 mg/kg lipopolysaccharide in mice except the control group on the 7th day. The results showed that magnolol and honokiol could reduce the diarrhea index and the level of pro-inflammatory cytokine interleukin-6, relieve the symptoms of enteritis, improve the intestinal morphology and restore the balance of intestinal microflora. Protein kinase B (AKT), inhibitor of apoptosis in B cell lymphoma (BCL-XL) and interleukin-18 receptor 1 (IL-18R1) were potential therapeutic targets for inflammation. Magnolol played an anti-inflammatory role by upregulating AKT, BCL-XL and the activating phosphatidylinositol 3 kinase-protein kinase (BPI3K-Akt) signaling pathway. On the contrary, the anti-inflammatory mechanism of honokiol involves down-regulating inflammation-related genes, including IL-18R1 and cyclic adenosine monophosphate effector element binding protein (CREB), thus inhibiting the tumor necrosis factor (TNF) signaling pathway. The study indicates that the appropriate dosage of magnolol, honokiol and honokiol is 100 mg/kg for relieving and treating intestinal injury. [ABSTRACT FROM AUTHOR]

To investigate the effects of honokiol on proliferation and apoptosis of human adipose-derived mesenchymal stem cells(hADSCs), and to investigate the effect of the drug on the tumor microenvironment. Methods hADSCs were incubated with different concentrations of honokiol, the proliferation of hADSCs was detected by MTS and Trypan blue staining, and cell apoptosis was assessed by annexin V/PI double staining. In the meantime, expression of mRNA and protein related to cell proliferation and apoptosis were detected by qPCR and Western blot, respectively. The expression of total MEK, phosphorylated MEK, total ERK and phosphorylated ERK proteins in the MEK-ERK1/2 signaling pathway were detected by Western blot. Results The effect of honokiol on inhibiting proliferation and promoting apoptosis of hADSCs was significantly enhanced with the increase of concentration. The expressions of proliferation-related genes CCND1, MKI67 and PCNA were down-regulated. The expressions of pro-apoptotic genes BAX and TP53 was up-regulated, and the expressions of anti-apoptotic gene BCL2 was down-regulated. Honokiol inhibited MEK and ERK1/2 phosphorylation in a concentration-dependent manner. Conclusions Honokiol inhibits proliferation and promotes apoptosis of hADSCs, and the specific mechanism is potentially related to the inhibition of MEK-ERK1/2 pathway. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Chinese Institute of Food Science & Technology / Zhongguo Shipin Xuebao is the property of Journal of Chinese Institute of Food Science & Technology Periodical Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Hydrobiology / Shuisheng Shengwu Xuebao is the property of Editorial Department of Journal of Hydrobiology and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective: To elucidate the definite role of silent information regulator 1(SIRT1)/Forkhead box protein O1(FOXO1)signaling pathway in the protective effects of honokiol(HKL) against brain injury in septic mice. Methods: Adult C57 BL/6 mice were subjected to cecal ligation and puncture(CLP) to induce sepsis-associated encephalopathy. The mice were randomly divided into six groups: Sham group, HKL group, CLP group, CLP+HKL group, CLP+HKL+EX527(a selective SIRT1 inhibitor) group and CLP+EX527 group. Forty-eight hours after the surgery, the brain water content, apoptotic ratio and the expression levels of SIRT1,Ac-FOXO1, Bax, Bcl-2, cleaved Caspase-3, IL-1β and TNF-α in each group were measured. Results: Compared with the CLP group,HKL significantly increased the expression level and the deacetylase activity of SIRT1 and the expression level of Bcl-2. HKL reduced brain water content, apoptotic ratio and the expression levels of Bax, cleaved Caspase-3, IL-1β and TNF-α when compared with the CLP group. However, these cerebral-protective effects of honokiol were largely abolished by EX527. Conclusions: HKL attenuates sepsis-associated encephalopathy by reducing apoptosis and inflammation through the activation of SIRT1/FOXO1 signaling pathway. [ABSTRACT FROM AUTHOR]

Copyright of Practical Pharmacy & Clinical Remedies is the property of Editorial Department of Practical Pharmacy & Clinical Remedies and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Practical Pharmacy & Clinical Remedies is the property of Editorial Department of Practical Pharmacy & Clinical Remedies and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective: To find quorum sensing inhibitors (QSIs) from Chinese herbal medicine Magnolia officinalis and to evaluate its inhibitory activity. Method: Pseudomonas aeruginous QSIS-lasI biosensor was used to monitor quorumsensing inhibitory activity. The bioactive compound in M. officinalis with anti-QS activity was separated by a bioautographic TLC assay, preparative TLC, and HPLC analysis. Its structure was identified by spectroscopic analysis. The pyocyanin and rhamnolipid production were determined by spectrophotometric method and orcinol method, respectively. And the swarming motility was assayed on semisolid agar plates. The effect of mRNA of QS-regulated gene was measured by RT-PCR. Results: M. officinalis extract was found to inhibit QS-controlled gene expression in P. aeruginous QSIS-lasI Biosensor. The active compound was purified and identified as honokiol. Honokiol at sub-inhibitory concentrations inhibited the production of virulence factors, including pyocyanin, rhamnolipid and swarming motility. It significantly reduced the level of mRNA of QS-related genes (P<0.05). Conclusion: Honokiol is a new QS inhibitor, which could be a potential agent for the treatment of bacterial infections. [ABSTRACT FROM AUTHOR]

【目的】 探讨和厚朴酚(HNK)对白血病细胞系U937细胞增殖和凋亡的影响65377;【方法】 将U937细胞和正常外周血单核细胞分别与HNK共培养,Hoechst33342荧光染色检测细胞凋亡形态,用噻唑蓝比色法(MTT)检测HNK对细胞增殖的抑制作用;流式细胞仪检测凋亡;罗丹明123检测线粒体膜电位;Caspase3/7活性检测试剂盒检测Caspase3/7活性;荧光定量PCR(FQ-PCR)检测Caspase-365380;Caspase-7 mRNA水平变化65377;【结果】 HNK对U937的体外增殖有显著抑制作用,48 h半数抑制浓度(IC50)为11.8 μg/mL,而对正常外周血单核细胞的IC50为40.3 μg/mL,Annexin V/PI双标染色显示,细胞凋亡与和厚朴酚呈浓度和时间依赖相关65377;HNK明显降低U937细胞线粒体膜电位,增加Caspase3/7活性及mRNA表达水平,但对正常外周血单核细胞的增殖抑制和凋亡作用不明显65377;【结论】 HNK可能通过激活caspase-3/7抑制U937细胞增殖65380;诱导U937细胞凋亡65377;