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Acute liver injury can be caused by chemicals and can lead to liver failure. We investigated the protective effect of helicid (HEL) on acute liver injury caused by CCl4 in mice. We found that ALT and AST levels as well as hepatic pathological damage in mice treated with CCl4 was increased significantly, while the effects were decreased by HEL treatment. HEL treatment increased the activity of T-SOD, GSH and CAT and reduced the level of MDA in CCl4 treated mice. HEL improved the histopathology of liver caused by CCl4. HEL also reduced TNF-α, IL-1β and IL- 6 activity caused by CCl4. We investigated the phosphorylation of p65 and IκB protein and found that HEL can alleviate liver damage via the NF-κB signaling pathway. Our findings indicate that HEL protects against acute liver injury induced by CCl4. The protective effect of HEL appears to be due to its antioxidative and anti-inflammatory properties through the NF-κB signaling pathway. [ABSTRACT FROM AUTHOR]

Oroxylin A, a natural flavonoid isolated from Scutellaria baicalensis, has been reported to have anti-inflammatory and antioxidant effects. However, suppression of oxidative stress and neuroapoptosis by oroxylin A is largely uninvestigated. To investigate the protective effects of oroxylin A, PC12 cells were exposed to oroxylin A and hydrogen peroxide solutions and measured. Oroxylin A significantly reduced the levels of intracellular calcium and reactive oxygen species and increased the levels of CAT and Mn/SOD. Oroxylin A also inhibited the activation of caspase-3. These results suggest that treatment of PC12 cells with oroxylin A inhibits H2O2-induced oxidative stress. [ABSTRACT FROM AUTHOR]

Context: Ginsenoside Rh2, an active component of ginseng, exhibits immunoregulatory and anti-inflammatory properties. Rh2-B1, a sulfated derivative, was prepared to enhance its water solubility. We studied the effect of Rh2-B1 on CTLL-2, a CD8+ cytotoxic T cell line that was known for protecting against viral infection. Objective: We aimed to investigate the effect of Rh2-B1 on interferon (IFN)-γ production and cell proliferation and its possible mechanism. Materials and methods: Enzyme-linked immunosorbent assay (ELISA) was employed to analyze the IFN-γ concentration of the whole blood and the supernatant of CTLL-2 cell culture. Cell proliferation assay was conducted using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Western blots were used to evaluate changes in signal transduction pathways in CTLL-2 cells. Results: Rh2-B1 was able to enhance IFN-γ production from whole blood culture of Balb/c mice. We then evaluated the effect of Rh2-B1 on a cytotoxic T cell line, CTLL-2 for cell proliferation, IFN-γ production and its molecular mechanism. Rh2-B1 promoted cell proliferation and IFN-γ production of CTLL-2 cells. It also induced activation of p38 mitogen-activated protein kinase (MAPK) and extracellular-signal-regulated kinases (ERK), but inhibited p56 Lck and transducer and activator of transcription 5 (STAT5) expression. The effect was blocked by the specific p38 MAPK inhibitor SB203580 and ERK inhibitor U0126. Conclusion: Rh2-B1 could stimulate cell proliferation and IFN-γ production by activating the p38 MAPK- and ERK-dependent signaling pathways in cytotoxic T cells. This may be a novel medicine for treatment of viral infections. [ABSTRACT FROM AUTHOR]

The article presents a study of screening of Chinese medical formula for treatment of chicken colibacillosis. Results of two repeated tests demonstrated that no. 4, 5, 24, and 26 had better effect on reducing the infected chicken mortality, showing stable effects on chicken infected by avian pathogenic Escherichia coli (APEC).

Xiang-Qi-Tang (XQT) is a Chinese herbal formula containing Cyperus rotundus, Astragalus membranaceus and Andrographis paniculata. Alpha-Cyperone (CYP), astragaloside IV (AS-IV) and andrographolide (AND) are the three major active components in this formula. XQT may modulate the inflammatory or coagulant responses. We therefore assessed the effects of XQT on lipopolysaccharide (LPS)-induced inflammatory model of rat cardiac microvascular endothelial cells (RCMECs). XQT, CYP, AS-IV and AND inhibited the production of tumor necrosis factor alpha (TNF-α), intercellular cell adhesion molecule-1 (ICAM-1) and plasminogen activator inhibitor-1 (PAI-1), and up-regulated the mRNA expression of Kruppel-like factor 2 (KLF2). XQT and CYP inhibited the secretion of tissue factor (TF). To further explore the mechanism, we found that XQT, or its active components CYP, AS-IV and AND significantly inhibited extracellular signal-regulated kinase (ERK), c-jun NH2-terminal kinase (JNK) and p38 phosphorylation protein expression as well as decreased the phosphorylation levels of nuclear factor κB (NF-κB) p65 proteins in LPS-stimulated RCMECs. These results suggested that XQT and its active components inhibited the expression of inflammatory and coagulant mediators via mitogen-activated protein kinase (MAPKs) and NF-κB signaling pathways. These findings may contribute to future research on the action mechanisms of this formula, as well as therapy for inflammation- or coagulation-related diseases. [ABSTRACT FROM AUTHOR]

The article presents a study which determines the different concentrations effects of ginsenoside Rh2-B2 on murine 1 RAW264.7 macrophages by tumor necrosis factor-α (TNF-α) and NF-κB signaling pathway induced by LPS in vitro.

The article presents a research which explores the possible effect of the 17-β-estradiol on the β-defensin expression in the epithelial cells found in the sheep's fallopian tubes.

The article presents a study of the antiviral effects of ginsenoside to Marek's disease virus. Oral ginsenoside was administered to chicks infected with Marek's disease virus. Pathological progress was mild in ginsenoside than in the viral control group as observed in gross inspection and electron microscope.

The article presents a study that evaluates the preventive effects of Ginkgolide A on patients with acute lung injury caused by lipopolysaccharide (LPS) in mice wherein the results show that Ginkgolide A attenuates LPS-induced pulmonary inflammation.

An abstract of the article "Adjuvant effect of sustained-release injection of Venenum bufonis," by Wu Shuai-Cheng and colleagues is presented.

The article presents a research which investigates the possible suppressive effect of Ginsenoside Rh2 to the MSB-1 cells by using flow cytometry.

Acute liver injury can be caused by chemicals and can lead to liver failure. We investigated the protective effect of helicid (HEL) on acute liver injury caused by CCl 4 in mice. We found that ALT and AST levels as well as hepatic pathological damage in mice treated with CCl 4 was increased significantly, while the effects were decreased by HEL treatment. HEL treatment increased the activity of T-SOD, GSH and CAT and reduced the level of MDA in CCl 4 treated mice. HEL improved the histopathology of liver caused by CCl 4 . HEL also reduced TNF-α, IL-1β and IL- 6 activity caused by CCl 4 . We investigated the phosphorylation of p65 and IκB protein and found that HEL can alleviate liver damage via the NF-κB signaling pathway. Our findings indicate that HEL protects against acute liver injury induced by CCl 4 . The protective effect of HEL appears to be due to its antioxidative and anti-inflammatory properties through the NF-κB signaling pathway.