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1.
J Pharm Pharmacol ; 74(1): 124-130, 2022 Jan 05.
Article in English | MEDLINE | ID: mdl-34559876

ABSTRACT

OBJECTIVE: To investigate whether the silent information regulator 1 (SIRT1) was involved in the protective effects of Ganoderma lucidum polysaccharides (GLP) against sepsis-induced cardiac dysfunction. METHODS: Lipopolysaccharide (LPS)-induced sepsis model was constructed in C57/BL6J mice. Mice were randomly divided into LPS + GLP + EX-527, LPS + EX-527, LPS + GLP, LPS or control group). The levels of serum inflammatory factor markers were examined by ELISA. H&E staining was performed to assess the inflammation. TUNEL staining and bromodeoxyuridine staining were used to observe cell apoptosis and proliferation, respectively. Expression of apoptosis and proliferation-related proteins was detected by western blot. KEY FINDINGS: GLP treatment could significantly increase the expression of SIRT1, reduce levels of serum inflammatory factors (TNF-α, IL-1α and IL-6) and inflammatory cells in mice heart tissue of sepsis models (all Ps < 0.01). Compared with LPS group, GLP treatment inhibited apoptosis and promoted proliferation of myocardial tissues (all Ps < 0.01). Besides, EX-527 (SIRT1 inhibitor) treatment could partially reverse the protective effects of GLP against sepsis-induced cardiac dysfunction (all Ps < 0.01). CONCLUSIONS: GLP might play a protective role in sepsis-induced cardiac dysfunction through regulating inflammatory response, apoptosis and proliferation via activating SIRT1. Therefore, GLP is expected to be a probable novel strategy for treatment of sepsis.


Subject(s)
Gene Expression Regulation/drug effects , Heart Diseases , Polysaccharides/pharmacology , Reishi , Sirtuin 1/metabolism , Animals , Apoptosis/drug effects , Heart Diseases/drug therapy , Heart Diseases/etiology , Inflammation/drug therapy , Inflammation/metabolism , Mice , Protective Agents/pharmacology , Sepsis/complications , Signal Transduction/drug effects
2.
Zhonghua Wai Ke Za Zhi ; 46(9): 694-6, 2008 May 01.
Article in Chinese | MEDLINE | ID: mdl-18956726

ABSTRACT

OBJECTIVE: To investigate the effects on lymphangiogenesis and angiogenesis of orthotopic implantation of lung cancer in nude mice with antisense oligonucleotides of VEGF-C. METHODS: The model in nude mice was established with orthotopic implantation for the human lung cancer cell line A549. Thirty nude mice were randomized into three groups: PBS control group, sense oligonucleotides control group and antisense oligonucleotides group (AODN group). After treatments were completed, the expression of VEGF-C and lymphatic microvessel density (LMVD) and microvessel density (MVD) of lung cancer were detected by RT-PCR,Western Blot and immunohistochemistry. RESULTS: The expression of VEGF-C in AODN group was inhibit significantly (P < 0.05). The LMVD in AODN group was decreased significantly (P < 0.1). Though the MVD in AODN group was also decreased, but there were no significant differences compared with control groups (P > 0.05). CONCLUSIONS: The antisense oligonucleotides of VEGF-C can inhibit the expression of VEGF-C in nude mice of orthotopic implantation of lung cancer. It could inhibit the lymphangiogenesis.


Subject(s)
Lung Neoplasms/pathology , Oligonucleotides, Antisense/pharmacology , Vascular Endothelial Growth Factor C/genetics , Animals , Cell Line, Tumor , Disease Models, Animal , Female , Humans , Liposomes , Lung Neoplasms/metabolism , Lymphangiogenesis/drug effects , Mice , Mice, Inbred BALB C , Mice, Nude , Microvessels/pathology , Neovascularization, Pathologic/drug therapy , Random Allocation , Transfection , Vascular Endothelial Growth Factor C/metabolism , Xenograft Model Antitumor Assays
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