Rosavin Alleviates LPS-Induced Acute Lung Injure by Modulating the TLR-4/NF-κB/MAPK Singnaling Pathways.

Acute lung injury (ALI) is a serious inflammatory disease with high morbidity and mortality. Rosavin is an anti-inflammatory and antioxidant phenylpropanoid and glucoside, which is isolated from Rhodiola rosea L. However, its potential molecular mechanisms and whether it has protective effects against lipopolysaccharide (LPS)-induced ALI remain to be elucidated. To assess the in vitro anti-inflammatory effects and anti-lung injury activity of rosavin, RAW264.7 and A549 cells were stimulated using 1 µg/mL LPS. Rosavin attenuated LPS-induced activation of the TLR-4/NF-κB signaling pathway in RAW264.7 cells and inhibited LPS-induced release of inflammatory factors in A549 cells. A mouse model of acute lung injury was constructed by intraperitoneal injection of 5 mg/kg LPS to observe the therapeutic effect of rosavin. Transcriptomics analysis and Western blot assays were utilized to verify the molecular mechanism, rosavin (20, 40, and 80 mg/kg) dose-dependently ameliorated histopathological alterations, reduced the levels of inflammatory factors, and inhibited the TLR-4/NF-κB/MAPK signaling pathway and apoptosis activation. Rosavin is a promising therapeutic candidate for acute lung injury by inhibiting the TLR-4/NF-κB/MAPK pathway.

Acute pancreatitis associated with pleural effusion: MDCT manifestations and anatomical basis.

BACKGROUND: Acute pancreatitis (AP) is a severe condition with complications that can impact multiple organ systems throughout the body. Specifically, the diffusion of peripancreatic effusion to the pleural cavity is a significant phenomenon in AP. However, its pathways and implications for disease severity are not fully understood. OBJECTIVE: This study aims to investigate the anatomical routes of peripancreatic effusion diffusion into the pleural cavity in patients with AP and to analyze the correlation between the severity of pleural effusion (PE) and the computed tomography severity index (CTSI) and acute physiology and chronic health evaluation II (APACHE II) scoring system. METHODS: 119 patients with AP admitted to our institution were enrolled in this study (mean age 50 years, 74 male and 45 female). Abdominal CT was performed, and the CTSI and APACHE II index were used to evaluate the severity of the AP, Meanwhile, the prevalence and semiquantitative of PE were also mentioned. The anatomical pathways of peripancreatic effusion draining to pleural were analyzed. Finally, the correlation relationship between the severity of AP and the PE was analyzed. RESULTS: In 119 patients with AP, 74.8% of patients had PE on CT. The anatomic pathways of peripancreatic effusion draining to pleural included esophageal hiatus in 33.7% of patients, aortic hiatus in 6.7% of patients and inferior vena cava hiatus in 3.37% of patients. The rating of PE on CT was correlated with CTSI scores (r= 0.449, P= 0.000) and was slightly correlated with the APACHE II scores (r= 0.197, P= 0.016). CONCLUSION: PE is a common complication of AP, which can be caused by anatomic pathways such as diaphragmatic hiatus. Due to its correlation with the CTSI score, the PE may be a supplementary indicator in determining the severity of AP.

Encoding and Decoding of p53 Dynamics in Cellular Response to Stresses.

In the cellular response to stresses, the tumor suppressor p53 is activated to maintain genomic integrity and fidelity. As a transcription factor, p53 exhibits rich dynamics to allow for discrimination of the type and intensity of stresses and to direct the selective activation of target genes involved in different processes including cell cycle arrest and apoptosis. In this review, we focused on how stresses are encoded into p53 dynamics and how the dynamics are decoded into cellular outcomes. Theoretical modeling may provide a global view of signaling in the p53 network by coupling the encoding and decoding processes. We discussed the significance of modeling in revealing the mechanisms of the transition between p53 dynamic modes. Moreover, we shed light on the crosstalk between the p53 network and other signaling networks. This review may advance the understanding of operating principles of the p53 signaling network comprehensively and provide insights into p53 dynamics-based cancer therapy.

The Amomum tsao-ko Essential Oils Inhibited Inflammation and Apoptosis through p38/JNK MAPK Signaling Pathway and Alleviated Gentamicin-Induced Acute Kidney Injury.

The clinical application of gentamicin may lead to acute kidney injury (AKI), and the nephrotoxicity of gentamicin is related to the pathological mechanism of several oxidative and inflammatory cytokines. Plant-derived essential oils have good anti-inflammatory and antioxidant properties. This study aimed to clarify the protective effect of Amomum tsao-ko essential oils (AOs) on gentamicin-induced AKI in rats and its possible mechanism. The rat AKI model was induced by intraperitoneal injection of gentamicin. After 14 days of oral AO treatment, the renal function and pathological changes of the kidney tissues were evaluated, and the level of kidney tissue oxidative stress was detected. The content of inflammatory cytokines was measured by ELISA. The expression of ERK1/2, JNK1/2, p38, NF-κB, caspase-3, and Bax/Bcl-2 proteins were estimated by Western blot analysis. The results showed that taking AO reduced the contents of serum urea and creatinine in AKI rats and improve the pathological changes and oxidative stress of the kidney tissue in rats. At the same time, AO reduced inflammation and apoptosis during AKI by regulating the MAPK pathway. The data show that AO has a protective effect on the kidneys and may be a potential drug for treating kidney injury.

Regulation of epithelial-to-mesenchymal transition in hypoxia by the HIF-1α network.

Epithelial-to-mesenchymal transition (EMT) plays a significant role in cancer metastasis. A series of models have focused on EMT regulation by TGF-ß network. However, how EMT is regulated under hypoxia is less understood. We developed a model of HIF-1α network to explore the potential link between EMT and the network topology. Our results revealed that three positive feedback loops, composed of HIF-1α and its three targets SNAIL, TWIST, and miR-210, should be sequentially activated to induce EMT under aggravating hypoxia. We suggested that the number of the positive feedback loops is critical for determining the number of stable states in EMT. Our work may advance the understanding of the significance of network topology in the regulation of EMT.

Autophagy inhibition via Becn1 downregulation improves the mesenchymal stem cells antifibrotic potential in experimental liver fibrosis.

Liver fibrosis (LF) is the result of a vicious cycle between inflammation-induced chronic hepatocyte injury and persistent activation of hepatic stellate cells (HSCs). Mesenchymal stem cell (MSC)-based therapy may represent a potential remedy for treatment of LF. However, the fate of transplanted MSCs in LF remains largely unknown. In the present study, the fate and antifibrotic effect of MSCs were explored in a LF model induced by CCl4 in mouse. Additionally, MSCs were stimulated in vitro with LF-associated factors, tumor necrosis factor-α (TNF-α), interferon-γ (IFN-γ), and transforming growth factor-ß1 (TGF-ß1), to mimic the LF microenvironment. We unveiled that MSCs exhibited autophagy in response to the LF microenvironment through Becn1 upregulation both in vivo and in vitro. However, autophagy suppression induced by Becn1 knockdown in MSCs resulted in enhanced antifibrotic effects on LF. The improved antifibrotic potential of MSCs may be attributable to their inhibitory effects on T lymphocyte infiltration, HSCs proliferation, as well as production of TNF-α, IFN-γ, and TGF-ß1, which may be partially mediated by elevated paracrine secretion of PTGS2/PGE2 . Thus, autophagy manipulation in MSCs may be a novel strategy to promote their antifibrotic efficacy.

Treatment with MQA, a Derivative of Caffeoylquinic Acid, Provides Neuroprotective Effects against Cerebral Ischemia Through Suppression of the p38 Pathway and Oxidative Stress in Rats.

1,5-O-dicaffeoyl-3-O-(4-malic acid methylester)-quinic acid (MQA), extracted from Arctium lappa L., has been observed to exert neuroprotective effects in vitro. The aim of this study was to investigate whether MQA is an effective therapeutic method for cerebral ischemic injury in vivo. In this study, adult male rats were randomly divided into four groups: a normal group, a model group subjected to middle cerebral artery occlusion (MCAO) for 24 h, a model + MQA group (which received intragastric MQA for the 7 days prior to MCAO), and a model + positive drug group. MQA appeared to induce effects in cerebral ischemic injury in rats, by downregulating malondialdehyde, glutathione peroxidase, and nitric oxide synthase levels. Treatment with MQA significantly reduced infarcted sections. In addition, caspase-3 and Iba1 protein expression were evaluated with immunohistochemistry, and cortical cell apoptosis was assessed with terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assays. Expression of AKT and Bax, ERK1/2, P38 and Bcl-2, NFkB1, PARP, and caspase-3 was assessed with Western blotting. We found Bcl-2 and NFkB1 (p50) expressions were upregulated, whereas the expression of PARP, caspase-3, NFkB1 (p105), ERK1/2, P38, AKT, and Bax was downregulated. In conclusion, we observed MQA was an effective treatment for cerebral ischemic injury in rats.

New ingol-type diterpenes from the latex of Euphorbia resinifera.

Two new ingol-type diterpenes, euphoresins A-B (1-2), have been isolated from the methanol extract of Euphorbium, the latex of Euphorbia resinifera Berg. Their structures were established on the basis of extensive analyses of their HR-ESI-MS, IR, UV, 1D, and 2D NMR spectra. The absolute configurations were confirmed by Mosher's method and circular dichroism (CD) analyses. The two compounds were tested for their cytotoxic activities against MCF-7, U937, and C6 cancer cell lines, but they both exhibited little cytotoxic effect.

[Triterpenoids from Uygur medicine latex of Euphorbia resinifera].

Ten triterpenes compounds were isolated from the methanol extraction of the latex of Euphorbia resinifera by means of various chromatographic methods such as silica gel, ODS and semi-preparative HPLC, Their structures were identified by spectroscopic methods and physicochemical properties. These isolated compounds were identified as 3ß-hydroxy-25,26,27-trinor eupha-8-ene-24-oate (1), iso-maticadienediol (2), 25,26,27-trinorTirucall-8-ene-3ß-ol-4-acid (3), dammarendiol Ⅱ (4), eupha-8,24-diene-3-ol-26-al (5), lnonotusane C (6), eupha-8,24-diene-3ß-ol-7,11-dione (7), inoterpene A (8), inoterpene B (9), and eupha-24-methylene-8-ene-3ß-ol-7,11-dione (10). Among them, compound 1 was a new natural product, compounds 2-4 were firstly isolated from the Euphorbiaceae and compounds 5 and 6 were isolated from the genus Euphorbia for the first time. The cytotoxicity of the compounds 1-10 against MCF-7, U937 and C6 cancer cell lines was evaluated, but none of the compounds was active.

Protective effects of Foeniculum vulgare root bark extract against carbon tetrachloride-induced hepatic fibrosis in mice.

AIM: To investigate the protective effects of Foeniculum vulgare root bark (FVRB), a traditional Uyghur medicine, against carbon tetrachloride (CCl4)-induced hepatic fibrosis in mice. METHODS: Mice were randomly divided into eight groups (n = 20 each). Except for the normal control group, mice in the rest groups were intraperitoneally injected (i.p.) with 0.1% CCl4-olive oil mixture at 10 mL/kg twice a week to induce liver fibrosis. After 4 wk, mice were treated concurrently with the 70% ethanol extract of FVRB (88, 176, 352 and 704 mg/kg, respectively) daily by oral gavage for 4 wk to evaluate its protective effects. Serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), triglyceride (TG), hexadecenoic acid (HA), laminin (LN), glutathione (GSH), superoxide dismutase (SOD), and malondialdehyde (MDA) in liver tissues were measured. Hematoxylin-eosin (H and E) staining and Masson trichrome (MT) staining were performed to assess histopathological changes in the liver. The expression of transforming growth factor ß1 (TGF-ß1), matrix metalloprotein 9 (MMP-9) and metallopeptidase inhibitor 1 (TIMP-1) was detected by immunohistochemical analysis. Additionally, TGF-ß1 and alpha-smooth muscle actin (α-SMA) protein expression was measured by Western blot. RESULTS: A significant reduction in serum levels of AST, ALT, TG, HA and LN was observed in the FVRB-treated groups, suggesting that FVRB displayed hepatoprotective effects. Also, the depletion of GSH, SOD, and MDA accumulation in liver tissues was suppressed by FVRB. The expression of TGF-ß1, MMP-9 and TIMP-1 determined by immunohistochemistry was markedly reduced in a dose-dependent manner by FVRB treatment. Furthermore, protective effects of FVRB against CCl4-induced liver injury were confirmed by histopathological studies. Protein expression of TGF-ß1 and α-SMA detected by Western blot was decreased by FVRB treatment. CONCLUSION: Our results indicate that FVRB may be a promising agent against hepatic fibrosis and its possible mechanisms are inhibiting lipid peroxidation and reducing collagen formation in liver tissue of liver fibrosis mice.

Preventive Effects of Rhodiola rosea L. on Bleomycin-Induced Pulmonary Fibrosis in Rats.

Rhodiola rosea L. (RRL) possesses a wide range of pharmacological properties, including lung-protective activity, and has been utilized in folk medicine for several 100 years. However, the lung-protective mechanism remains unclear. This study investigated the possible lung-protective activity mechanism of RRL in a pulmonary fibrosis (PF) rat model. Lung fibrotic injury was induced in Sprague-Dawley rats by single intratracheal instillation of saline containing bleomycin (BLM; 5 mg/kg). The rats were administered 125, 250, or 500 mg/kg of a 95% ethanol extract of RRL for 28 days. The animals were killed to detect changes in body weight, serum levels of glutathione (GSH) and total superoxide dismutase (T-SOD), as well as lung tissue hydroxyproline (HYP) content. Tumor necrosis factor-α (TNF-α), transforming growth factor-ß1 (TGF-ß1), and interleukin 6 (IL-6) levels were measured in bronchoalveolar lavage fluid (BALF) by enzyme-linked immunosorbent assay. Hematoxylin and eosin, Masson's trichrome, and immunohistochemical staining were performed to observe the histopathological changes in lung tissues. Additionally, target-related proteins were measured by Western blotting. RRL alleviated the loss of body weight induced by instilling BLM in PF rats, particularly at the 500 mg/kg per day dose. RRL reduced HYP (p < 0.01) and increased GSH and T-SOD contents. BALF levels of TNF-α, TGF-ß1, and IL-6 decreased significantly in the RRL-treated groups. Expression levels of matrix metalloproteinase-9 (MMP-9) and α-smooth muscle actin decreased significantly in a dose-dependent manner in response to RRL. Moreover, the levels of TGF-ß1 and tissue inhibitor of metalloproteinase-1 in lung tissues also decreased in the RRL-treated groups. RRL alleviated BLM-induced PF in rats. Our results reveal that the protective effects of RRL against fibrotic lung injury in rats are correlated with its anti-inflammatory, antioxidative, and anti-fibrotic properties. MMP-9 may play important roles in BLM-induced PF.

Human recombinant endostatin Endostar attenuates hepatic sinusoidal endothelial cell capillarization in CCl4­induced fibrosis in mice.

The aim of the present study was to detect the effect of the recombinant human endostatin Endostar on hepatic sinusoidal capillarization in CCl4­induced murine models of liver fibrosis. The liver fibrosis model was induced in BALB/c mice using intraperitoneal injection of CCl4 for 6 weeks. Animals were divided into the following six treatment groups: Group 1, normal animals; group 2, CCl4­induced liver fibrosis; group 3, CCl4+Endostar 20 mg/kg/day for 6 weeks; group 4, CCl4+Endostar 10 mg/kg/day for 6 weeks; group 5, CCl4+Endostar 20 mg/kg/day for 4 weeks; and group 6, CCl4+Endostar 10 mg/kg/day for 4 weeks. The average number of fenestrae per hepatic sinusoid was determined using transmission electron microscopy. Vascular endothelial growth factor (VEGF) and VEGF receptor (VEGFR) 1 and 2 expression was detected by western blot analysis. There were significant differences in the number of fenestrae per sinusoid between the normal control and untreated model fibrotic mice (P<0.01), and between the untreated model and Endostar­treated mice (P<0.05). Endostar treatment was associated with reduced levels of VEGFR1 and VEGFR2 in liver tissues (P<0.01), as well as with decreased hepatic sinusoidal endothelial cell capillarization in CCl4­induced mouse models of liver fibrosis, and this effect may involve the VEGF pathway. However, further studies are required to confirm its involvement in other causes of liver fibrosis.

Untangling knots between autophagic targets and candidate drugs, in cancer therapy.

Autophagy is an evolutionarily conserved lysosomal mechanism implicated in a wide variety of pathological processes, such as cancer. Autophagy can be regulated by a limited number of autophagy-related genes (Atgs) such as oncogenic Bcl-2/Bcl-XL , mTORC1, Akt and PI3KCI, and tumour suppressive proteins PI3KCIII, Beclin-1, Bif-1, p53, DAPKs, PTEN and UVRAG, which play their crucial roles in regulating autophagy-related cancer. As autophagy has a dual role in cancer cells, with tumour-promoting and tumour-suppressing properties, it has become an attractive target for a series of emerging small molecule drugs. In this review, we reveal new discoveries of related small molecules or chemical compounds that can regulate autophagic pathways and lead to pro-death or pro-survival autophagy, in different types of cancer. We discuss the knots between autophagic targets and candidate drugs, in the hope of shedding new light on exploiting new anti-tumour small molecule drugs for future cancer therapy.

Constituents from Zhuyeqing Liquor with hepatoprotective effect on alcohol-induced HepaG 2 toxicity.

An unprecedented new skeleton compound (1R, 10R, 11S)-10,11-dimethyl-4-formyl-2,9-dioxa-bicyclo [5.4.0] undeca-4,6-dien-3-one (1), monoterpenoids and monoterpene glycoside picrocrocinic ester (2), epijasminoside B (3) and 6'-O-(3-methoxyl-4-hydroxyl-coumaroyl)-epijasminoside B (4), along with 26 known compounds, were obtained from Zhuyeqing Liquor. These compounds were identified mainly by analyzing their NMR, HR-ESI-MS and CD data. The isolated compounds were screened against alcohol induced HepaG 2 toxicity for hepatoprotective assay. Compounds 10, 19, 21 and 26 displayed the highest potency against alcohol induced HepaG 2 toxicity with the cell viability ratio 41.21, 56.91, 67.69 and 70.32% respectively.

Endostar, a novel human recombinant endostatin, attenuates liver fibrosis in CCl4-induced mice.

Decreasing hepatic fibrosis remains one of the major therapeutic challenges in hepatology. The present study aims to evaluate the effect of Endostar on both CCl4-induced liver fibrosis in mice and a hepatic stellate cell (HSC) line. Two main models were studied: (i) a liver fibrosis model was induced in BALB/c mice using CCl4 by intraperitoneal injection for six weeks. Six animal groups were studied: group 1: normal animals; group 2: CCl4-induced liver fibrosis; group 3: CCl4 + Endostar 20 mg/kg/d, six weeks; group 4: CCl4 + Endostar 10 mg/kg/d, six weeks; group 5: CCl4 + Endostar 20 mg/kg/d, four weeks; group 6: CCl4 + Endostar 10 mg/kg/d, four weeks corresponded to different Endostar doses and duration of administration. Liver fibrosis was evaluated by histopathological staining and liver hydroxyproline content. Expressions of collagen type I, α-smooth muscle actin (α-SMA), TGF-ß1 and VEGFR were measured by real-time polymerase chain reaction (PCR). (ii) A liver cell model. HSC-T6 cells were cultured with or without Endostar for 12 h or 24 h. Expressions of collagen type I, α-SMA, and TGF-ß1 were measured by real-time PCR. Collagen I and transforming growth factor ß1 (TGF-ß1) contents in cell supernatant were measured by enzyme-linked immunosorbent assay. As compared to the group without Endostar, liver fibrosis scores and hydroxyproline content were decreased in both Endostar groups (P < 0.05). Moreover, Endostar inhibited the hepatic expression of α-SMA, TGF-ß1, Collagen-1, VEGFR1, and VEGFR2 mRNA (P < 0.05). In the HSC-T6 cell line model, Endostar profoundly inhibited the expression of α-SMA, Collagen-1, and TGF-ß1 mRNA. Expressions of Collagen-1 and TGF-ß1 protein were decreased in the Endostar group as compared to the normal controls in the supernatant of HSC-T6 cells (P < 0.05). Endostar decreased both liver fibrosis in CCl4-induced mice and collagen synthesis in HSCs in vitro. Therefore, this recombinant human endostatin is a promising compound for counteracting liver fibrosis.

Two new compounds from Bombyx batryticatus.

Two new compounds beauvericins M1 (1) and S1 (2) were isolated from Bombyx batryticatus. Their structures were established as (3α,6α)-3-benzyl-6-secbutyl-4-methylmorpholine-2,5-dione (1) and (5α,8α)-epidioxyergosterol-24-one-6,22-dien-3ß-ol (2) by various spectroscopic techniques including 1D NMR ((1)H NMR and (13)C NMR), 2D NMR (HSQC, HMBC, (1)H-(1)H COSY, NOESY), and HR-ESI-TOF-MS.

Two new phthalides with BuChE inhibitory activity from Ligusticum chuanxiong.

Two new phthalides, chuanxiongdiolides A and B, were isolated from the roots of Ligusticum chuanxiong Hort. Their structures were established by UV, IR, 1D (¹H, ¹³C) and 2D (HSQC, ¹H-¹H COSY, HMBC, NOESY) NMR, and HR-ESI-MS methods, and their absolute configurations were assigned via circular dichroism exciton chirality. The two compounds showed different degrees of inhibitory effects against butyrylcholine esterase.

Protective effect of Zhuyeqing liquor, a Chinese traditional health liquor, on acute alcohol-induced liver injury in mice.

The study first evaluated the hepatoprotective effect of Zhuyeqing Liquor (ZYQL) against acute alcohol-induced liver injury in mice. Animals were administered orally with 50% alcohol 12 ml/kg at 4 h after the doses of ZYQL everyday for fourteen consecutive days except mice in normal group. The protective effect was evaluated by biochemical parameters including serum aspartate transaminase (AST), alanine transferase (ALT), total-bilirubin (TBIL) and reduced glutathione (GSH), malondialdehyde (MDA), superoxide dismutase (SOD) in liver tissue. The result were confirmed histopathologically and the expression of TNF-α in mice liver was determined by immunohistochemistry analysis. HPLC-PDA was used for phytochemical analysis of ZYQL, and the plant source of each compound was claritied by UPLC-TOF-MS. The result showed that pretreatment with ZYQL exhibited a significant protective effect by reversing the biochemical parameters and histopathological changes in a dose depended manner. HPLC analysis indicated that ZYQL contained flavonoids, iridoids, terpenoids and phenolic acids, which might be the active chemicals. This study demonstrated the hepatoprotective activity of ZYQL, thus scientifically supported the function of its health care.

Protective effects of Zhuyeqing liquor on the immune function of normal and immunosuppressed mice in vivo.

BACKGROUND: Zhuyeqing Liquor (ZYQL), a well-known Chinese traditional health liquor, has various biological properties, including anti-oxidant, anti-inflammatory, immunoenhancement and cardiovascular protective effects. METHODS: The protective effects of Zhuyeqing Liquor (ZYQL) on the immune function was investigated in vivo in normal healthy mice and immunosuppressed mice treated with Cyclophosphamide (Cy, 100 mg/kg) by intraperitoneal injection on days 4, 8 and 12. ZYQL (100, 200 and 400 mg/kg) was administered via gavage daily for 14 days. The phagocytotic function of mononuclear phagocytic system was detected with carbon clearance methods, the levels of interleukin-6 (IL-6) and interferon-gamma (IFN-γ) in serum were detected with Enzyme linked immunosorbent assay (ELISA). Immune organs were weighed and organ indexes (organ weight/body weight) of thymus and spleen were calculated. Meanwhile, the activity of lysozyme (LSZ) in serum and the activity of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT) in spleen tissue were measured. RESULTS: ZYQL significantly upgrades the K value for clearance of carbon particles in normal mice treated with ZYQL (400 mg/kg) and immunosuppressed mice treated with ZYQL (100, 200 and 400 mg/kg) together with Cy (100 mg/kg) in vivo. The treatment of ZYQL (100, 200 and 400 mg/kg) effectively increased the activity of serum lysozyme as well as promoted the serum levels of IL-6 and IFN-γ in normal mice and immunosuppressed mice. Furthermore, ZYQL (100, 200 and 400 mg/kg) had an antioxidant effects in immune system by enhancing the antioxidant enzyme activity of SOD, CAT and GSH-Px in vivo. In addition, ZYQL (100, 200 and 400 mg/kg) effectively elevated the Cy-induced decreased organ index (thymus and spleen). CONCLUSIONS: The present work shows that the dose-dependent administration of ZYQL is capable of influencing immune responses, which implying that its valuable functional health may be attributed partly to its protective effects for the immune function.

Two new terpenoid benzoates with antitumor activity from the roots of Ferula dissecta.

Two new sesquiterpene benzoates, syreiteate A (1) and syreiteate B (2), were isolated from the roots of Ferula dissecta (Ledeb.) Ledeb. Their structures were elucidated by extensive spectroscopic methods including 1D ((1)H and (13)C) NMR, 2D (HSQC, HMBC, DQF-COSY, and NOESY) NMR, and ESI-TOF-MS. Their configurations were determined on the basis of the analysis of the coupling constants, NOESY correlations, and circular dichroism spectrum. Compounds 1 and 2 showed potent growth inhibitory activity against cervical cancer HeLa cell line with the IC50 values of 13.2 and 19.3 µM, respectively.