Effects Of Ganoderma Lucidum Polysaccharides Research Articles

The effect of Ganoderma lucidum polysaccharide extract on sensitizing prostate cancer cells to flutamide and docetaxel: an in vitro study

Ganoderma lucidum polysaccharide is the most widely used complementary therapy in cancer. The present study aims to investigate the possible interaction between Ganoderma lucidum polysaccharide and Docetaxel (a chemotherapy drug) and the first-line medication for prostate cancer treatment (Flutamide) and sensitizing the cells to these treatments. The cytotoxic effects of Ganoderma lucidum polysaccharide in combination with Docetaxel and Flutamide on prostate cancer cells were investigated by the MTT test, Hoechst staining, and flow cytometry. In addition, the expression of genes related to apoptosis, angiogenesis, Epithelial-Mesenchymal Transition pathway (EMT), and prostate cancer biomarkers by Real-Time PCR was investigated. The results demonstrated that IC50 values for Ganoderma lucidum polysaccharide (30 μM and 20 μM), Docetaxel (10 μM and 5 μM), and Flutamide (20 μM and 12 μM) with MTT were confirmed by flow cytometry in a dose and time-dependent manner. Regarding the high efficacy of Ganoderma lucidum polysaccharide in combination with Flutamide and Docetaxel, 10 μM and 5 μM Flutamide were used instead of 20 μM and 12 μM and 5 μM and 2 μM Docetaxel was used instead of 10 μM and 5 μM in PC3 and LNCap, respectively. Moreover, for the first time, it was shown that Ganoderma lucidum polysaccharide alone and in combination with Docetaxel and Flutamide significantly augmented apoptosis, reduced cell migration and colonization, and downregulated expression of KLK2 and EMT pathway genes in both PC3 and LNCap cell line (P < 0.01). Ganoderma lucidum polysaccharide synergistically increased the effect of Docetaxel and Flutamide and increased the sensitivity of the prostate cancer cell lines to these drugs. Therefore, it may provide a new therapeutic strategy against prostate cancer.

Ganoderma lucidum polysaccharides associated with 5-Fluorouracil impair OSCC tumorigenesis in vitro

BackgroundsGanoderma lucidum polysaccharides have been shown several anti-cancer, anti-inflammatory, and immunomodulatory properties among studies with different tumor models and its use with advanced and conventional combination therapies is a world trend. The administration of 5-Fluorouracil is already used as chemotherapy for many tumors and works on tumor remission; however, its adverse effects are still severe, impoverishing treatment and quality of life for patients. Cancer stem cells represent a subpopulation of cells with defense mechanisms against chemotherapy agents and are the main cause of relapses and metastases in cancer treatments. Also, the Epithelial-Mesenchymal Transition program increases properties related to tumor malignancy and mortality. In this scenario, the aim of the study is to evaluate the effects of Ganoderma lucidum polysaccharides in combination with 5-Fluorouracil on the subpopulation of cancer stem cells present in the human oral squamous carcinoma cell line SCC-9. MethodsSCC-9 cells were treated in vitro for 72 h with different 5-Fluorouracil low doses, associated or not with Ganoderma lucidum polysaccharides. Cells maintained with culture media or cisplatin were used as control. All the cells were evaluated for cytotoxicity, cancer stem cells, and Epithelial-Mesenchymal Transition properties. ResultsThe associated treatment avoided proliferation, delayed migration, slightly modified morphology of cells, increased apoptosis, decreased colony and blocked spheres formation, and downregulated cancer stem cells, Epithelial-Mesenchymal Transition, and ABC drug transporters expression. In addition, Ganoderma lucidum polysaccharides + 5-Fluorouracil changed the treated cells into a non-cancer stem cell phenotype, a characteristically not resistant and less proliferative population. The 5-Fluorouracil treatment alone showed remarkable modification in cellular morphology, apoptosis, and absence of holoclones; however, it upregulated the molecular expression of cancer stem cells' hallmarks. ConclusionsThese findings demonstrate that combining Ganoderma lucidum polysaccharides with a low dose of 5-Fluorouracil is effective against oral squamous cell carcinoma in vitro by enhancing the cells' sensitivity to drugs and reducing the characteristics associated with cancer stem cells (CSCs). This suggests the possibility of reducing conventional chemotherapy doses and improving oral squamous cell carcinoma treatment. It also highlights the potential for this combination to be used as an adjunct in Complementary Alternative Medicine (CAM).

Potential Anti-Rheumatoid Arthritis Activities and Mechanisms of Ganoderma lucidum Polysaccharides

Rheumatoid arthritis (RA) is a chronic and autoimmune disease characterized by inflammation, autoimmune dysfunction, and cartilage and bone destruction. In this review, we summarized the available reports on the protective effects of Ganoderma lucidum polysaccharides (GLP) on RA in terms of anti-inflammatory, immunomodulatory, anti-angiogenic and osteoprotective effects. Firstly, GLP inhibits RA synovial fibroblast (RASF) proliferation and migration, modulates pro- and anti-inflammatory cytokines and reduces synovial inflammation. Secondly, GLP regulates the proliferation and differentiation of antigen-presenting cells such as dendritic cells, inhibits phagocytosis by mononuclear macrophages and nature killer (NK) cells and regulates the ratio of M1, M2 and related inflammatory cytokines. In addition, GLP produced activities in balancing humoral and cellular immunity, such as regulating immunoglobulin production, modulating T and B lymphocyte proliferative responses and cytokine release, exhibiting immunomodulatory effects. Thirdly, GLP inhibits angiogenesis through the direct inhibition of vascular endothelial cell proliferation and induction of cell death and the indirect inhibition of vascular endothelial growth factor (VEGF) production in the cells. Finally, GLP can inhibit the production of matrix metalloproteinases and promote osteoblast formation, exerting protective effects on bone and articular cartilage. It is suggested that GLP may be a promising agent for the treatment of RA.

Gastroprotective Effects of Ganoderma lucidum Polysaccharides with Different Molecular Weights on Ethanol-Induced Acute Gastric Injury in Rats.

Ganoderma lucidum is known as a medicine food homology that can ameliorate gastrointestinal diseases. To evaluate the gastroprotective effects on different Ganoderma lucidum polysaccharides (GLPs), GLP was separated into three parts with different molecular weights using 100 kDa, 10 kDa, and 1 kDa membranes. The mitigation effects of different GLPs on ethanol-induced acute gastric injury were observed in rats. After pretreatment with different GLPs, especially GLP above 10 kDa, the symptoms of gastric mucosal congestion and bleeding were improved; serum myeloperoxidase, inflammatory factor, and histamine were decreased; and antioxidant activity and defense factors (NO and EGF) were increased. Results showed that GLP with different molecular weights had a dose-dependent effect in alleviating alcohol-induced gastric injury. The underlying mechanism might be related to regulating anti-oxidation, promoting the release of related defense factors, reducing inflammatory factors, and reducing the level of histamine in serum. The current work indicated that GLPs above 10 kDa could be applied as natural resources for producing new functional foods to prevent gastric injury induced by ethanol.

Effect of &amp;lt;i&amp;gt;Ganoderma lucidum&amp;lt;/i&amp;gt; Polysaccharide on Antioxidative Ability of Rats with Myocardial Injury Induced by Doxorubicin

Objective: The objective is to investigate the effect of Ganoderma lucidum polysaccharide (GLPS) on the oxidative stress induced by doxorubicin (DOX) in cardiomyocytes. Methods: SD rats were divided into control group, DOX group, GLPS low dose and high dose + DOX group. SOD and MDA levels in myocardial tissue were detected in each group. The expression of related proteins in each group was detected by Western blot. Results: GLPS can increase the SOD level and decrease MDA caused by DOX (p < 0.05). GLPS can reduce the increase of p53 content caused by DOX (p < 0.05), and up regulate the antioxidant enzyme HO-1 (p < 0.05), MDM2 (p < 0.05) and Nrf2 (p < 0.05). Conclusion: Ganoderma polysaccharide can improve the oxidative stress injury of myocardial tissue induced by doxorubicin and play a protective role in myocardial tissue.

Ganoderma lucidum polysaccharides protect against sepsis-induced cardiac dysfunction by activating SIRT1.

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. 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. 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). 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.

Neuroprotective Effect of Ganoderma lucidum Polysaccharides in an Epileptic Rat Model

We have previously shown the antiepileptic effects of Ganoderma lucidum polysaccharides in in vitro studies; however, so far there is no such study reported in an in vivo model. In this study, the status epilepticus was induced in rats by kainic acid injection followed by G. lucidum polysaccharides treatment once a day for 7 days. Their epileptic behavior, electroencephalograph, along with the expression of caveolin-1, brain derived neurotrophic factor, nuclear factor kappa B, and hippocampal neuronal survival were assessed. Results showed that the epileptic behavior was improved significantly after G. lucidum polysaccharides treatments by a significant reduction of both the epileptic score and the duration of a heavy seizure attack while increasing both the epileptic latency and the time to heavy seizure attack. The epileptic electroencephalograph was ameliorated from previous sharp waves and frequent high amplitudes spikes to a group of scattering waves with lower frequency and small spikes. Furthermore, G. lucidum polysaccharides treatments enhanced the expression of caveolin-1, brain derived neurotrophic factor, and survivin, but decreased nuclear factor kappa B expression. These changes indicate that G. lucidum polysaccharides can alleviate epileptic seizure and this neuroprotective effect may be via increasing the expression of caveolin-1, brain derived neurotrophic factor, and survivin and decreasing the expression of nuclear factor kappa B in the hippocampal neurons.

Effects of Ganoderma lucidum Polysaccharides on Different Pathways Involved in the Development of Spinal Cord Ischemia Reperfusion Injury: Biochemical, Histopathologic, and Ultrastructural Analysis in a Rat Model

Inflammation and oxidative stress are 2 important factors in the emergence of paraplegia associated with spinal cord ischemia-reperfusion injury (SCIRI) after thoracoabdominal aortic surgery. Here it is aimed to investigate the effects of Ganoderma lucidum polysaccharide (GLPS) on SCIRI. Rats were randomly selected into 4 groups of 8 animals each: sham, ischemia, methylprednisolone, and GLPS. To research the impacts of various pathways that are efficacious in formation of SCIRI, tumor necrosis factor α, interleukin 1β, nitric oxide, superoxide dismutase levels, and catalase, glutathione peroxidase activities, malondialdehyde levels, and caspase-3 activity were measured in tissues taken from the spinal cord of rats in all groups killed 24 hours after ischemia reperfusion injury. The Basso, Beattie, and Bresnahan locomotor scale and inclined plane test were used for neurologic assessment before and after SCIRI. In addition, histologic and ultrastructural analyses of tissue samples in all groups were performed. SCIRI also caused marked increase in tissue tumor necrosis factor α, interleukin 1β, nitric oxide, malondialdehyde levels, and caspase-3 activity, because of inflammation, increased free radical generation, lipid peroxidation, and apoptosis, respectively. On the other hand, SCIRI caused significant reduction in tissue superoxide dismutase, glutathione peroxidase, and catalase activities. Pretreatment with GLPS likewise diminished the level of the spinal cord edema, inflammation, and tissue injury shown by pathologic and ultrastructural examination. Pretreatment with GLPS reversed all these biochemical changes and improved the altered neurologic status. These outcomes propose that pretreatment with GLPS prevents progression of SCIRI by alleviating inflammation, oxidation, and apoptosis.

UPLC-MS-based serum metabolomics reveals protective effect of Ganoderma lucidum polysaccharide on ionizing radiation injury

Ethnopharmacological relevanceGanoderma lucidum Polysaccharide (GLP),traditional Chinese medicine (TCM) active ingredient, has a long history and has good curative effects on radiation injury. However, the mechanism of GLP treating radiation injury has not been clearly elucidated. The aim of the studyThis study was aimed to investigate the preventive effects of GLP on mice with radiation injury and to explore its mechanisms by serum metabolomics. Materials and methodsThirty mice were randomly divided into three groups,and namely 10 per group. The normal control group and the radiation model with normal saline and GLP group with GLP treatment (96 mg·kg-1) for 14 days. 2 h after 7th day after the intragastric administration, the model group and GLP group were subjected to whole body irradiation by X-rays except the normal control group. The peripheral blood WBC, RBC, HGB, PLT indicators.UPLC-Q-TOF-MS technique was used to analyze the serum of normal group, model group and GLP group, and to explore its potential key biomarkers and corresponding related metabolic pathways. ResultsThe number of peripheral blood leukocytes (WBC) in the radiation model group was lower than that in the GLP group and the number of platelets (PLT) in the GLP group was significantly higher than that in the model group.Combined with the methods of principal component analysis (PCA), projection to latent structure-discrimination analysis (PLS-DA), three group were clearly distinguished from each other and 18 metabolites were identified as the potential biomarkers in the GLP treated mice. The identified biomarkers indicated that there were perturbations of the taurine and hypotaurine metabolism and glycerophospholipid metabolism. ConclusionGLP can play a role in radiation protection by improving the expression of related potential biomarkers and related metabolic pathways in serum of radiation-induced mice.

Ganoderma lucidum Polysaccharide (GLP) Inhibited the Progression of Oral Squamous Cell Carcinoma via the miR-188/BCL9/β-Catenin Pathway

Objective. The effects of Ganoderma lucidum polysaccharide (GLP) on the proliferation and migration of oral squamous cell carcinoma (OSCC) cells (HSC-3) were investigated in this study. Methods. Oral squamous cell carcinoma (OSCC) cells (HSC-3) were cultured in vitro and were treated with different concentrations of GLP. CCK-8 assay and scratch assay were then used to detect the inhibitory effect of GLP on these cells. qRT-PCR and western blot were used to measure the expression changes of the genes involved in the miR-188 and β-catenin signaling pathways. Results. GLP had significant cytotoxicity to HSC-3 cells and was capable of inhibiting the proliferation and migration of HSC-3 cells. GLP upregulated the expression of miR-188 in HSC-3 cells and via which inhibited the proliferation and migration of HSC-3 cells. In addition, miR-188 inhibited the activation of the β-catenin signaling pathway through its target BCL9. Conclusions. GLP inhibited the proliferation and migration of OSCC cells (HSC-3) by regulating the miR-188/BCL9/β-catenin signaling pathway. The results in this study provided a theoretical basis for the treatment of OSCC with GLP.

Lingzhi or Reishi Medicinal Mushroom, Ganoderma lucidum (Agaricomycetes), Polysaccharides Suppressed Adipogenesis and Stimulated Lipolysis in HPA-v and 3T3-L1 Adipocytes.

Ganoderma lucidum polysaccharides (GLP) are one of the major bioactive components with many beneficial properties. In the present study we aimed to systematically evaluate the effects of GLP on lipid metabolism in human (HPA-v) and murine adipocytes (3T3-L1). Cell viability was assessed by MTT assay. Lipid accumulation in mature adipocytes were evaluated by ORO staining and quantified using the triglyceride (TG) assay. Lipolysis was investigated by measuring the free glycerol released in the cell culture medium after treatments. The mRNA and protein levels of key genes regulating lipid metabolism were determined by qRT-PCR and western blotting in HPA-v cells. ORO staining showed that GLP suppressed lipid accumulation similarly in both HPA-v and 3T3-L1 cells. TG assay confirmed that GLP significantly inhibited cell differentiation (p < 0.001). The lipolysis assay showed that GLP enhanced triglyceride hydrolysis in both adipocytes (p < 0.05). GLP stimulated AMPK phosphorylation, which promoted the phosphorylation of ACC1, its downstream target. qRT-PCR and western blotting showed that the genes encoding transcription factors for adipocyte differentiation (PPARγ, C/EBPα, and SREBPlc) and certain adipogenic genes (ACC1, PLIN1, and FASN) were downregulated (p < 0.05). The lipolytic gene HSL was upregulated and highly phosphorylated (activated) at mRNA and protein levels, respectively, upon GLP treatment. These results suggested that GLP possessed beneficial antiadipogenic effects and can potentially be developed into antiobesity products.

Ganoderma lucidum polysaccharide reduces melanogenesis by inhibiting the paracrine effects of keratinocytes and fibroblasts via IL-6/STAT3/FGF2 pathway.

Our previous study found that Ganoderma lucidum polysaccharide (GLP), bioactive ingredients from Ganoderma lucidum, protected fibroblasts from photoaging. However, whether GLP can affect melanogenesis in melanocytes through regulating paracrine mediators that secreted by keratinocytes and fibroblasts is unclear. We aimed to investigate the efficacy and mechanisms of action of GLP in melanogenesis by regulating paracrine effects of keratinocytes and fibroblasts. The effect of GLP on cell viability affected by GLP was measured by the 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay. After an immortal keratinocyte line (HaCaT) and primary fibroblasts (FB) were treated with GLP, the supernatants of HaCaT and FB cells were collected and cocultured with an immortalized melanocyte line (PIG1). The expression levels of melanogenesis-associated genes in PIG1 cells were measured by quantitative real-time polymerase chain reaction (qRT-PCR) and western blot analysis. Furthermore, FRS-2, ERK, JNK, and p38 phosphorylation levels were measured. Then, major melanogenic paracrine mediators in HaCaT and FB cells treated with GLP were evaluated by qRT-PCR and enzyme-linked immunosorbent assay (ELISA). In addition, the expression of IL-6 and STAT3 was examined in HaCaT and FB cells. GLP was not cytotoxic to HaCaT and FB cells. The supernatants of GLP-treated HaCaT and FB cells downregulated the expression levels of MITF, TYR, TYRP1, TYRP2, RAB27A, and FSCN1 genes and inhibited the phosphorylation of FRS-2, ERK, JNK, and p38 in PIG1 cells. GLP also decreased FGF2 secretion in HaCaT and FB cells. Moreover, GLP reduced IL-6 expression and STAT3 phosphorylation in HaCaT and FB cells. GLP reduced melanogenesis in melanocytes by inhibiting the paracrine effects of keratinocytes and fibroblasts via IL-6/STAT3/FGF2 pathway.

Evaluating the effect of Ganoderma lucidum polysaccharides on five cytochrome P450 isozymes with cocktail probe drugs in rats by LC–MS/MS

Ganoderma lucidum polysaccharides (GLPs) are commonly used as health-promoting medicine and dietary supplement due to the positive effects in immune modulation, antitumor and antioxidant activities. However, whether GLPs executes other uncharacterized effects is largely unclear. The rats were pre-primed with GLPs and then administrated with canonical “cocktail probes” of cytochrome P450 (CYP450) isozymes including caffeine, tolbutamide, dextromethorphan, omeprazole, and midazolam. The plasma concentrations of probes at each indicated time point were simultaneously detected using the designed high-performance liquid chromatography-tandem mass spectrometric (LC-MS/MS) method. The results suggested that GLPs could increase the accumulated levels of caffeine, tolbutamide and midazolam in plasma as compared to control group. Besides, GLPs reduced the concentration of dextromethorphan in blood at high dose, while elevated it at low dose. GLPs could inhibit the activities of CYP1A2, and CYP3A4, additionally; GLPs at low dose suppressed the activity of CYP2D6, which demonstrated that drugs co-administrated with GLPs might require strictly evaluating the dose relation.

Anti-Inflammatory and Hepatoprotective Effects of Ganoderma lucidum Polysaccharides against Carbon Tetrachloride-Induced Liver Injury in Kunming Mice

Background: Ganoderma lucidum Polysaccharides (GLPS) were found to possess various pharmacological properties including anti-inflammatory and hepatoprotective activities. However, the effect and possible mechanism of GLPS treatment on liver injury have not yet been reported. Therefore, this study aimed to explore the potential anti-inflammatory and hepatoprotective effects and possible mechanism of GLPS in carbon tetrachloride (CCl₄)-induced acute liver injury mice. Summary: GLPS significantly reduced the activation of NLRP3 inflammasome and improved liver function in liver injury mice. It significantly inhibited CCl₄-induced changes of alanine aminotransferase and aspartate aminotransferase activities in serum, as well as nitric oxide synthase (NOS) and cytochrome P450 2E1 (CYP2E1) activities in liver tissue; it also remarkably decreased levels of liver weight and index, total bilirubin, interleukin (IL)-1β, IL-18, IL-6 and tumor necrosis factor-α in serum, as well as malondialdehyde and IL-1β in liver tissue. Protein expression levels of liver NLRP3, ASC, and Caspase-1 were also downregulated, while the glutathione level in liver tissue was remarkably enhanced in GLPS groups compared to that of the model group. Key Message: These results suggested that GLPS may be a potential for the prevention and treatment of acute liver injury with liver inflammation. The possible mechanism may be related to the inhibition of free radical lipid peroxidation, NOS, and CYP2E1 activities and activation of liver inflammatory factors.

Article Effect and Mechanism of Ganoderma lucidum Polysaccharides on Human Fibroblasts and Skin Wound Healing in Mice.

To investigate the effects of Ganoderma lucidum polysaccharides (GL-PS) on human fibroblasts and skin wound healing in Kunming male mice and to explore the putative molecular mechanism. Primary human skin fibroblasts were cultured. The viability of fibroblasts treated with 0, 10, 20, 40, 80, and 160 μg/mL of GL-PS, respectively were detected by 3-4,5-dimethyl-2-thiazolyl-2,5-diphenyl-2-Htetrazolium bromide (MTT). The migration ability of fibroblasts treated with 0, 10, 20, and 40 μg/mL of GL-PS were measured by transwell assay. The secretion of the C-terminal peptide of procollagen type I (CICP) and transforming growth factor-β1 (TGF-β1) in the cell supernatant was tested by enzyme-linked immunosorbent assay. The expression of β-catenin was detected by Western blot. Furthermore, the Kunming mouse model with full-layer skin resection trauma was established, and was treated with 10, 20, and 40 mg/mL of GL-PS, respectively as external use. The size of the wound was measured daily, complete healing time in each group was recorded and the percentage of wound contraction was calculated. Compared with the control group, 10, 20, and 40 μg/mL of GL-PS significantly increased the viability of fibroblasts, promoted the migration ability of fibroblasts, and up-regulated the expressions of CICP and TGF-β1 in fibroblasts (Plt;0.05 or Plt;0.01). The expression of β-catenin in fibroblasts treated with 20 and 40 μg/mL of GL-PS was significantly higher than that of the control group (Plt;0.01). Furthermore, after external use of 10, 20, and 40 mg/mL of GL-PS, the rates of wound healing in mice were significantly higher and the wound healing time was significantly less than the control group (Plt;0.05 or Plt;0.01). A certain concentration of GL-PS may promote wound healing via activation of the Wnt/β-catenin signaling pathway and up-regulation of TGF-β1, which might serve as a promising source of skin wound healing.

Immunoexpression of Vascular Endothelial Growth Factor, &amp;#946;-cell Lymphoma 2 and Cluster of Differentiation 68 in Cerebellar Tissue of Rats Treated with Ganoderma lucidum

Traumatic brain injury (TBI) can potentially lead to hemorrhages in all areas of the skull, which can damage cells and nerve connections. This study aims to investigate the protective effects of Ganoderma lucidum polysaccharides (GLPS) as a antioxidant on cerebellar cell tissues after traumatic brain injury in rats. Sprague Dawley rats were subjected to TBI with a weight-drop device using 300 g1m weight-height impact. The groups are consisted of control, trauma, and trauma+Ganoderma lucidum groups. At seven days post-brain injury, experimental rats were decapitated after intraperitoneal administration of ketamine HCL (0.15 ml/100 g body weight). Cereballar samples were taken for histological examination or determination of malondialdehyde (MDA) and glutathione (GSH) levels and myeloperoxidase (MPO) activity. Significant improvement was observed in cells and vascular structures of Ganoderma lucidum treated groups when compared to untreated groups. It is believed that Ganoderma lucidum may have an effect on the progression of traumatic brain injury. Ganoderma lucidum application may affect angiogenetic development in blood vessel endothelial cells, decrease inflammatory cell accumulation by affecting cytokine mechanism and may create apoptotic nerve cells and neuroprotective mechanism in glial cells.

Molecular characterization of the effects of Ganoderma Lucidum polysaccharides on the structure and activity of bovine serum albumin.

The investigation about polysaccharides-protein system is attributed to numerous very important applications for pharmaceutical, food, chemical and other industries. In the present work, multi-spectral methods and molecular docking were used to analyze the molecular interactions of polysaccharides from Ganoderma Lucidum (GLP) with bovine serum albumin (BSA). The nonenzymatic glucosylation, fibrillation, thermal stability, and structure information of GLP-BSA system were also studied. The results showed that the formation of GLP-BSA complex by mainly hydrogen-bonding forces resulted in the conformational changes of protein. GLP acted as a stabilizer to increase the thermal stability of BSA solution having a novel and more stable conformational state during the thermal denaturation process. 8-anilino-1-naphthalenesulfonic acid (ANS) fluorescence spectral results suggested that there exist some intermediate state which has low binding ability with ANS in the presence of GLP. The presence of GLP caused a decrease in the formation of beta sheet structures with a lower rate. The fluorescence spectra of BSA glycosylated by GLP confirmed the formation of covalent bonds between BSA and GLP through the Maillard reaction which was also confirmed by using thermogravimetric (TGA) and Fourier transform infrared (FTIR) analysis. In addition, BSA still maintains the esterase-like good activity in the presence of GLP. These results provide a basis for screening the molecular interactions of polysaccharides with protein from the perspective of important food active ingredients.

Effect of Ganoderma lucidum polysaccharides on oxidative damage in liver of STZ-diabetic rats

In this study, the effects of exogenic application of Ganoderma lucidum polysaccharide on oxidative stress and hyperlipidemia was determined in diabetics rats. The study included 60 Wistar albino rats aged 4-5 months. Rats were divided into 6 equal groups. The groups were control, Ganoderma lucidum polysaccharide, diabetic, diabetic+60 mg/kg polysaccharides, diabetic+120 mg/kg polysaccharides and diabetic+10 mg/kg polysaccharide. Diabetes was induced by intraperitoneal injection of streptozocine at the dose rate of 50 mg/kg. The rats were fed ad-libitum throughout the experiment. At the end of the study, we took some samples out of total oxidant and total antioxidant levels and measured them with the spectrophotometer; thereafter we used the auto-analyser to measure the levels of total cholesterol, triglycerides, HDL, LDL, VLDL cholesterol and pancreatic amylase. We examined the blood of diabetic fasting rats and the effect was that their glucose level was increased significantly. (p<0.05), nonetheless the dose of 60, 120 and 180 mg/kg of Ganoderma lucidum polysaccharides did not reduce the blood glucose level (p>0.05). With the diabetic rats, the dose of 60, 120 and 180 mg/kg of Ganoderma lucidum polysaccharides rides effected in the increase of serum levels of total cholesterol, triglycerides, VLDL, and HDL cholesterol levels, although it was not a significant change (p>0.05), instead, we observed a statistically significant decrease of LDL cholesterol level (p<0.05). According to this study we concluded that polysaccharides effects in the decrease of hyperlipidaemia with regard to diabetes. During the study we applied Ganoderma lucidum polysaccharides exogenously (60, 120, 180 mg/kg) and it did not affect the level of total antioxidant in diabetes significantly (p>0.05), however with a dose of 180 mg/kg the total oxidant level in pancreas and liver tissues was reduced significantly and has been considered as crucial fact. The collected data supported our view on histopathologic examination. Based on all the information, we used one type of fungus Ganoderma lucidum polysaccharides which did not influence the blood glucose level in diabetes, whereas with regard to LDL and total oxidants it played a significant role in reducing its levels.

Effects of Ganoderma lucidum polysaccharides against doxorubicin-induced cardiotoxicity

Doxorubicin (DOX) is a widely used anthracycline derivative anticancer drug, but the use of DOX in clinical applications is limited by its cardiotoxicity. In the current research, we were aiming to assess the effects of Ganoderma lucidum polysaccharides (GLPS) on DOX-induced cardiotoxicity and to illustrate the associated mechanisms. H9c2 rat cardiomyocytes were treated with DOX in the absence or presence of GLPS, and we found GLPS treatment ameliorated DOX-induced H9c2 cell death. Moreover, results of in vivo studies indicated that GLPS significantly decreased the serum levels of lactate dehydrogenase (LDH), creatine kinase (CK) and aspartate aminotransferase (AST) and attenuated DOX-induced histological changes of the heart tissues. In addition, we found DOX administration promoted myocardial apoptosis, potentiated oxidative stress, decreased the activities of antioxidant enzymes and increased the production of pro-inflammatory cytokines. However, GLPS pretreatment markedly attenuated all these untoward effects of DOX. Furthermore, GLPS pretreatment was found to inhibit Cul3-mediated K48-linked polyubiquitination of Nrf2 through suppressing Cul3 expression, thereby stabilizing Nrf2 expression in H9c2 cells after DOX treatment, leading to the decreased expression of P53 and p-P65 and increased levels of MDM2 and HO-1, resulted in the attenuated apoptosis, oxidative stress and inflammation induced by DOX.

Protective effect of Ganoderma lucidum polysaccharide against carbon tetrachloride-induced hepatic damage in precision-cut carp liver slices.

The aim of the present study was to investigate the protective effects of Ganoderma lucidum polysaccharide (GLPS) against carbon tetrachloride (CCl4)-induced hepatotoxicity in vitro in common carp. Precision-cut liver slices (PCLSs), which closely resemble the organ from which they are derived, were employed as an in vitro model system. GLPS (0.1, 0.3, and 0.6mg/ml) was added to PCLS culture system before the exposure to 12mM CCl4. The supernatants and slices were collected to detect molecular and biochemical responses to CCl4 and PCLS treatments. The levels of CYP1A, CYP3A, and CYP2E1 were measured by ELISA; the mRNA expressions of TNF-α, IL-1β, IL-6, and iNOS were determined by RT-PCR; and the relative protein expressions of c-Rel and p65 were analyzed by western blotting. Results showed that GLPS inhibited the elevations of the marker enzymes (GOT, GPT, LDH) and MDA induced by CCl4; it also enhanced the suppressed activity of antioxidant enzymes (SOD, CAT, GSH-Px, T-AOC). The treatment with GLPS resulted in significant downregulation of NF-κB and inflammatory cytokine mRNA levels and significant decreases in the hepatic protein levels of CYP1A, CYP3A, and CYP2E1. These results suggest that GLPS can protect CCl4-induced PCLS injury through inhibiting lipid peroxidation, elevating antioxidant enzyme activity, and suppressing immune inflammatory response.