Objective:To investigate the effect of Tongguan Fang drug-containing serum on LPS-induced inflammation of RAW264.7 cells,so as to clarify the cellular mechanism of the Tongguan Fang in treating tubal inflammatory infertility.Methods:Lipo-polysaccharide(LPS)was used to stimulate the RAW264.7 macrophage cell line as an in vitro model,Detected levels of cellular oxida-tive stress(ROS),apoptosis and expressions of PI3K/Akt signaling pathway proteins.CCK-8 was used to detect effect of Tongguan Fang drug-containing serum on cellular inflammation.Effects of Tongguan Fang-containing serum on cell inflammation were assessed using CCK-8 assay.Cells were divided into control group,LPS-induced inflammation model group,and Tongguan Fang-containing serum-treated LPS-induced inflammation model groups of different concentrations.qPCR was performed to detect mRNA expression levels of IL-1β,IL-6 and TNF-α in different groups.Immunofluorescence and Western blot were used to evaluate phosphorylation levels of the PI3K/Akt signaling pathway and protein levels of Bcl-2,Bax and caspase-3 of apoptotic.Hoechst 33342/PI staining and flow cytometry were employed to assess the impact of Tongguan Fang-containing serum on cell apoptosis.DCFH-DA probe was used to measure cellular ROS levels affected by Tongguan Fang-containing serum.Results:①Tongguan Fang-containing serum reduced LPS-induced cellular injury in a dose-dependent manner;②Tongguan Fang-containing serum decreased production of pro-inflammatory cytokines IL-6,IL-1β and TNF-α induced by LPS;③Tongguan Fang-containing serum reduced intracellular ROS generation induced by LPS;④Pre-treatment with Tongguan Fang-containing serum activated PI3K/Akt signaling pathway;⑤Tongguan Fang-containing serum promoted cell apoptosis.Conclusion:Treatment with Tongguan Fang-containing serum can reduce cellular injury and inflam-mation,protect cells from LPS-induced cellular injury by activating the PI3K/Akt signaling pathway and promoting cell apoptosis,and further alleviate cellular inflammation levels.

Objective:To investigate the effect of Tongguan Fang drug-containing serum on LPS-induced inflammation of RAW264.7 cells,so as to clarify the cellular mechanism of the Tongguan Fang in treating tubal inflammatory infertility.Methods:Lipo-polysaccharide(LPS)was used to stimulate the RAW264.7 macrophage cell line as an in vitro model,Detected levels of cellular oxida-tive stress(ROS),apoptosis and expressions of PI3K/Akt signaling pathway proteins.CCK-8 was used to detect effect of Tongguan Fang drug-containing serum on cellular inflammation.Effects of Tongguan Fang-containing serum on cell inflammation were assessed using CCK-8 assay.Cells were divided into control group,LPS-induced inflammation model group,and Tongguan Fang-containing serum-treated LPS-induced inflammation model groups of different concentrations.qPCR was performed to detect mRNA expression levels of IL-1β,IL-6 and TNF-α in different groups.Immunofluorescence and Western blot were used to evaluate phosphorylation levels of the PI3K/Akt signaling pathway and protein levels of Bcl-2,Bax and caspase-3 of apoptotic.Hoechst 33342/PI staining and flow cytometry were employed to assess the impact of Tongguan Fang-containing serum on cell apoptosis.DCFH-DA probe was used to measure cellular ROS levels affected by Tongguan Fang-containing serum.Results:①Tongguan Fang-containing serum reduced LPS-induced cellular injury in a dose-dependent manner;②Tongguan Fang-containing serum decreased production of pro-inflammatory cytokines IL-6,IL-1β and TNF-α induced by LPS;③Tongguan Fang-containing serum reduced intracellular ROS generation induced by LPS;④Pre-treatment with Tongguan Fang-containing serum activated PI3K/Akt signaling pathway;⑤Tongguan Fang-containing serum promoted cell apoptosis.Conclusion:Treatment with Tongguan Fang-containing serum can reduce cellular injury and inflam-mation,protect cells from LPS-induced cellular injury by activating the PI3K/Akt signaling pathway and promoting cell apoptosis,and further alleviate cellular inflammation levels.

Abstract OBJECTIVE To investigate the effect and mechanism of flavonoids from Sophora flavescens Ait. on testicular tissue damage in male mice induced by local heat stress in the scrotum. METHODS TCMSP database was used to screen the targets of flavonoids in Sophora flavescens Ait., and the bioinformatics analysis was performed on the target. The mouse model of scrotal heat stress was used and the flavonoids of Sophora flavescens Ait. was used for intervention. The sperm density and sperm aberration rate of mice in each group were measured, and the morphological changes of testicular tissue were observed. Tumor necrosis factor-α (TNF-α) and interleukin 17(IL-17) mRNA and protein levels in testicalar were detected of by q-PCR and Western blotting. Na+-K+-ATPase, Mg2+-ATPase, Ca2+-ATPase, lactate dehydrogenase(LDH), sorbitol dehydrogenase(SDH) activity, malondialdehyde (MDA), NO, TNF-α level and the content of testosterone in serum were detected in tissue homogenate. RESULTS Heat stress could lead to the decrease of sperm density and increase of aberrant sperm, the obvious thinning of testicular spermatogenic epithelium, the decrease of cell level and quantity, the significant decrease of ATPase, LDH, SDH activities, and the increase of MDA, NO content, TNF-α and IL-17 expression in testicular tissue. After the intervention with 250, 500 mg·kg-1·d-1 flavonoids of Sophora flavescens Ait., the quality of sperm and the damage of testicular tissue morphology were improved. The level of TNF-α and IL-17 in serum and testicular tissue were decreased, and the activity of ATPase, SDH and the level of testosterone were increased. CONCLUSION The mechanism of flavonoids of Sophora flavescens Ait. is through inhibiting the inflammatory factor TNF-α and IL-17 levels, improve the anti-lipid peroxidation ability and inhibite the role of NO, enhance the activity of energy enzymes in spermatogenesis, improve the level of serum testosterone, and improve the reproductive disorders caused by heat stress.

Objective: To evaluate the inhibitory effect of dihydroartemisinin on neuroblastoma cell line SH-SY5Y, explore the possible mechanism of dihydroartemisinin against neuroblastoma cells. Methods: The cell viability of dihydroartemisinin treated SH-SY5Y cells was examined by MTT assay and morphology of cells was observed by using inverted microscope. Cell cycle was examined with flowcytometry assay, then cyclin D1 and caspase-3 proteins expression was detected by ELISA and western blotting assay. Results: MTT analysis results showed that cell viability significantly decreased after exposure to 0.05, 0.50, 5.00 and 50.00 μmol/L dihydroartemisinin in a dose-dependent manner, and the lower density of cells was observed in treated groups. The number of cells in sub-G1 phase was increased after treatment with different doses of dihydroartemisinin compared with the control group. The expression of cyclin D1 protein was decreased, while the expression of caspase-3 protein was increased in treated group. Conclusions: Dihydroartemisinin could inhibit the proliferation through stopping the cell cycle and inducing the apoptosis in neuroblastoma SH-SY5Y cells.

OBJECTIVETo detect the effect and mechanism of procyanidin foom vaccinium (PC) on myocardial fibrosis in rats.

METHODThe myocardial fibrosis model in rats was built by subcutaneous injection of 5 mg x kg(-1) x d(-1) of isoprenaline (Iso) for 7 days in vivo while intragastrically administrating PC 100, 200 and 400 mg x kg(-1) x d(-1) for 14 days. Following the model was established, myocardial indexes (heart weight/body weight, HW/BW and left ventricalar weight/body weight, LVW/BW) were measured. Besides, angiotensin II and I , III collagen quantification levels in blood serum were determined respectively by ELISA. The change in the content of nitric oxide (NO) in blood serum was determined with colorimetry. The content of malondialdehyde (MDA) in left ventricle was assayed with spectrophotometry. The contents of lactate dehydrogenase (LDH) and creatine kinase (CK) in blood serum were detected with automatic biochemistry analyzer.

RESULTCompared with the control group, the myocardial indexes, the contents of I , III collagen quantification, angiotensin II in blood serum and malondialdehyde in left ventricle were markedly increased and the content of nitric oxide in blood serum was decreased, the contents of lactate dehydrogenase and creatine kinase in blood serum were markedly increased in Iso model group (P<0.05 or P<0.01). Compared with the model group, the myocardial indexes were decreased, the contents of I , III collagen quantification, angiotensin II in blood serum were reduced in PC 200 and 400 mg x kg(-1) x d(-1) groups (P<0.05 or P<0.01). The content of nitric oxide in blood serum was increased, the content of malondialdehyde in left ventricle was markedly decreased, the contents of lactate dehydrogenase and creatine kinase in blood serum were markedly decreased in PC three groups (P<0.05 or P<0.01).

CONCLUSIONPC could inhibit collagen synthesis by decreasing angiotensin II level and increasing the content of nitric oxide and antioxidation, and thereby inhibiting myocardial fibrosis and protect myocardium in rats.

Angiotensins ; blood ; Animals ; Antioxidants ; administration & dosage ; pharmacology ; Biflavonoids ; administration & dosage ; pharmacology ; Catechin ; administration & dosage ; pharmacology ; Endomyocardial Fibrosis ; chemically induced ; drug therapy ; metabolism ; Female ; Isoproterenol ; adverse effects ; Male ; Malondialdehyde ; metabolism ; Nitric Oxide ; blood ; Proanthocyanidins ; administration & dosage ; pharmacology ; Rats ; Rats, Wistar ; Vaccinium ; chemistry ; Ventricular Remodeling ; drug effects

OBJECTIVETo explore effect of Qindan Fuzheng Capsule (QFC) on ultrastructure of cardiomyocytes and hepatocytes injured by high microwave radiation in rats.

METHODSEighteen adult Wistar rats were equally divided into 3 groups in random: rats in Group A were untreated as the normal control, rats in Group B received 6 min microwave radiation (100 mW/cm2 high power) to cause injury of cardiomyocytes and hepatocytes, and Group C received the same radiation but treated with QFC perfusion, 2 mL (equivalent to 4.75 g crude drug) once a day, for 7 successive days, starting from 6 h after radiation. All rats were sacrificed 7 days later, their fresh tissue of heart apex and right lobe of liver were taken and prepared to routine transmission electron microscopy specimen for ultrastructural observation.

RESULTSCompared with Group A, different degrees of ultrastructural changes on nuclei and organelle were observed in Group B and C, but the injury in Group C was significantly milder than that in Group B, showing normal sized cells with good structure approximate to the morphology in Group A.

CONCLUSIONSQFC showed protective effect on microwave radiation injured ultrastructural changes in rats' cardiomyocytes and hepatocyte. Its mechanism was possibly correlated with the suppression of lipid peroxidation and the improvement of metabolism in myocardial and hepatic cells.

Animals ; Drugs, Chinese Herbal ; pharmacology ; Female ; Hepatocytes ; drug effects ; ultrastructure ; Male ; Microwaves ; adverse effects ; Myocytes, Cardiac ; drug effects ; ultrastructure ; Rats ; Rats, Wistar

OBJECTIVETo observe the effects of schizandrins on the learning and memory disorder in mice, and explore its mechanism.

METHODThe memory impairment model was established by using the pentobarbital sodium (20 mg x kg(-1)) intraperitoneally injected in mice. Schizandrins (0.5, 1.0, 2.0 g x kg(-1)) were administered through intragavage for consecutive 14 days. Morris Water Maze test was used to evaluate the impairment of learning and memory. The energy of superoxide dismutase (SOD), nitric oxide (NO) and catalase (CAT) of brain tissue were measured. And the positive expression of nuclear transcription factor-kappaB p65 (NF-kappaB p65), caspase-3 in the hippocampus CA1 region were determined by immunohistochemical analysis. At the cellular level, 24 h after schizandrins (0.062 5, 0.125, 0.25 g x L(-1)) were pre-administered, the apoptosis model of PC12 cell was induced by H2O2, and activity of PC12 cell was detected by MTT colorimetric assay, the energy of NO in cell serum were measured. The expression of Bcl-2 was determined by the combination of immunocytochemical staining and image analysis software.

RESULTMorris Water Maze test showed that the model group mice took shorter searching time and distance on the previous flat area than those in the control group (P < 0.05), which could be prolonged after schizandrins treatment (P < 0.05, P < 0.01). Compared with the control group, the level of NO increased while the activity of SOD, CAT decreased in the model group (both P < 0.01). After treated with schizandrins, the level of NO significantly decreased (P < 0.01), while the activity of SOD increased (P < 0.01). Immunohistochemistry analysis showed that the protein expression of NF-kappaB p65, Caspase-3 in the hippocampal CA1 region significantly increased after modeling, while schizandrins (1.0 g x kg(-1)) can significantly inhibit the protein expression of NF-kappaB p65, Caspase-3 (P < 0.05, P < 0.01). Compared with the H2O2, model group, schizandrins (0.125, 0.25 g x L(-1)) can significantly increased PC12 cell activity and decreased the NO level (P < 0.05, P < 0.01), the expression of Bcl-2 in the schizandrins group (0.125, 0.25 g x L(-1)) was up-regulated.

CONCLUSIONSchizandrins could improve the learning-memory dysfunction induced by the sodium pentobarbital in mice, and its protective mechanism is related to the lowering oxidative damage and inhibiting the cell apoptosis through up-regulating the expression of Bcl-2.

Animals ; Apoptosis ; drug effects ; Behavior, Animal ; drug effects ; CA1 Region, Hippocampal ; metabolism ; Caspase 3 ; metabolism ; Cell Line ; Cyclooctanes ; pharmacology ; therapeutic use ; Disease Models, Animal ; Drugs, Chinese Herbal ; pharmacology ; therapeutic use ; Female ; Learning Disorders ; chemically induced ; drug therapy ; metabolism ; Lignans ; pharmacology ; therapeutic use ; Male ; Memory Disorders ; chemically induced ; drug therapy ; metabolism ; Mice ; Nitric Oxide ; metabolism ; Oxidative Stress ; PC12 Cells ; Polycyclic Compounds ; pharmacology ; therapeutic use ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; Rats ; Superoxide Dismutase ; metabolism ; Transcription Factor RelA ; metabolism

Inonotus obliquus has high nutritional and medicinal value, especially in treating malignant tumors, diabetes, cardiovascular disease and AIDS, attracting significant attention from scholars in recent years. In this paper, the biological characteristics, chemical composition and pharmacologic effects of Inonotus obliquus were summarized. And the applications in medicine and food were introduced. Future research on Inonotus obliquus was also discussed in order to make Inonotus obliquus obtain effective exploitation and satisfy people's demands.
Anti-Inflammatory Agents ; chemistry ; pharmacology ; therapeutic use ; Antineoplastic Agents ; chemistry ; pharmacology ; therapeutic use ; Antioxidants ; chemistry ; pharmacology ; therapeutic use ; Antiviral Agents ; chemistry ; pharmacology ; therapeutic use ; Basidiomycota ; chemistry ; Biomedical Research ; trends ; Drugs, Chinese Herbal ; chemistry ; pharmacology ; therapeutic use ; Humans ; Hypoglycemic Agents ; chemistry ; pharmacology ; therapeutic use ; Platelet Aggregation Inhibitors ; chemistry ; pharmacology ; therapeutic use ; Triterpenes ; chemistry ; isolation & purification

This project aimed to investigate the effect of taurine on nitric oxide (NO) and protein kinase C alpha (p-PKCalpha) in the proliferation of cultured neonatal rat cardiac fibroblast (CFb) induced by angiotensin II (Ang II), and to explore the effect of taurine on the signal transduction pathway in CFb proliferation. The cultured neonatal rats CFb were isolated by trypsin digestion method. The proliferation of CFb was induced by Ang II and detected by thiazole blue (MTT) colorimetric assay. The levels of collagen I and collagen III were measured by the ELISA. Cell cycle was analyzed by flow cytometry. The change of NO content was measured by nitric acid reductase method and the protein express of p-PKCalpha in cells was determined by Western blotting technology. Among the concentration of 40 - 160 mmol x L(-1), taurine could not only prevent the synthesis of collagen and the proliferation of CFb stimulated by angiotensin II, but also block CFb in the G0/G1 phase from entering the S phase, resulting in more cells in the G0/G1 phase and fewer in the S phase (P < 0.05, P < 0.01). Taurine significantly increased NO level and inhibited p-PKCalpha expression in CFb (P < 0.05, P < 0.01). The inhibitory effects of taurine on CFb proliferation and collagen synthesis might be due to inhibition of p-PKCalpha expression and NO content increase.
Angiotensin II ; pharmacology ; Animals ; Animals, Newborn ; Cell Cycle ; drug effects ; Cell Proliferation ; drug effects ; Cells, Cultured ; Collagen Type I ; metabolism ; Collagen Type III ; metabolism ; Fibroblasts ; cytology ; metabolism ; Myocytes, Cardiac ; cytology ; metabolism ; Nitric Oxide ; metabolism ; Protein Kinase C-alpha ; metabolism ; Rats ; Rats, Wistar ; Signal Transduction ; drug effects ; Taurine ; pharmacology