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Fig. 5 in Lanostane-type triterpenoids from the mycelial mat of Ganoderma lucidum and their hepatoprotective activities

Fig. 5. Effects of compounds 1, 6, and 8–10 (15 μM) on ALT activity (A), AST activity (B), LDH activity (C) and GSH level (D) in HepG2 cells. Results are expressed as the mean SEM (n 3). NAC was used as positive control (15 μM). (#) P <0.05 and (##) P <0.01 with respect to the normal group; (*) P <0.05 and (**) P <0.01 ± = with respect to the model group.

Fig. 4 in Lanostane-type triterpenoids from the mycelial mat of Ganoderma lucidum and their hepatoprotective activities

Fig. 4. Hepatoprotective effects of the indicated compounds against H2O2-induced injury in HepG2 cells. Compounds were used at 15 μM. Results are expressed as the mean SEM (n 4). NAC was used as positive control (15 μM). (##) P <0.01 with respect to the normal (untreated) group; (*) P <0.05 and (**) P <0.01 with ± = respect to the model (H2O2-treated) group.

Fig. 4 in Function of ceramide synthases on growth, ganoderic acid biosynthesis and sphingolipid homeostasis in Ganoderma lucidum

Fig. 4. Ganoderic acid biosynthesis in G. lucidum is influenced by the lag gene. A Systematic content analysis of ganoderic acid in the lag-silenced, WT and SiControl strains. B–D Relative gene expression of hmgr (B), sqs (C) and osc (D) in the WT, SiControl and lag-silenced strains. There are three independent biological replicates in each column. Error bars represent standard deviations, and asterisks show significant differences from control (WT and Sicontrol) strains according to Student's t-test (**P <0.01, n = 3).

Fig. 3 in Function of ceramide synthases on growth, ganoderic acid biosynthesis and sphingolipid homeostasis in Ganoderma lucidum

Fig. 3. Effect of lag gene silencing on G. lucidum growth. Morphology of fungal colonies in lag-silenced, WT and SiControl strains after cultivation in the dark on CYM medium at 28 ̊C for 5 days. Three independent biological replicates in each column. Error bars represent standard deviations, and asterisks show significant differences from control (WT and Sicontrol) strains according to Student's t-test (**P <0.01, n = 3).

Fig. 1 in Function of ceramide synthases on growth, ganoderic acid biosynthesis and sphingolipid homeostasis in Ganoderma lucidum

Fig. 1. Overview of the sphingolipid biosynthetic pathway in yeast and filamentous fungi. The abbreviations used are as follows: Dihydroxy LCB: dihydroxy longchain (sphingoid) base; Trihydroxy LCB: trihydroxy long-chain sphingoid base; Long chain FA-CoA: long chain fatty acyl-coenzyme A; Very long chain FA-CoA: very long chain fatty acyl-coenzyme A; IPC synthase: inositol phosphorylceramide synthase; IPC mannosyl transferase: inositol phosphorylceramide mannosyl transferase; MIPCs: mannose inositol phosphorylceramides; M (IP)2Cs: mannose (inositol phosphoryl)2- ceramides.

Fig. 2. G in Function of ceramide synthases on growth, ganoderic acid biosynthesis and sphingolipid homeostasis in Ganoderma lucidum

Fig. 2. G. lucidum harbours three ceramide synthases. Phylogenetic analysis of ceramide synthases in eukaryotes. The phylogenetic tree was conducted using MEGA 6 and can be roughly divided into three major groups: human, plant and fungi. The evolutionary history was inferred by the neighbour-joining method from 1000 replicates using MEGA 6.

Fig. 5 in Function of ceramide synthases on growth, ganoderic acid biosynthesis and sphingolipid homeostasis in Ganoderma lucidum

Fig. 5. Sphingolipid profiling of the lag-silenced, WT and SiControl strains. The relative amounts of Cer (A), GlcCer (B), IPC (C), MIPC (D) and M (IP)2C (E) in each strain. Comparison of the sphingolipid intensity ratios between the WT and lag-silenced strains. Each sphingolipid (Cer/GlcCer/IPC/ MIPC/M(IP)2C) intensity ratio was calculated as the percentage of the corresponding total sphingolipid detected in the WT or mutant. The sphingolipid species are indicated as the number of carbon atoms: the unsaturated bond number of the fatty acid: hydroxyl number. For example, Cer 32:0:2 = Cer (d18:0/14:0); Cer 36:0:3 = Cer (t18:0/18:0 or d18:0/18:0 (2-OH)); Cer 36:0:4 = Cer(t18:0/18:0 (2-OH)); Cer 38:1:2 = Cer (d18:0/20:1 or d18:1/ 20:0) and Cer 42:2:2 = (d18:0/24:2, d18:2/24:0 or d18:1/24:1). There are three independent biological replicates in each column. Error bars represent standard deviations, and asterisks show significant differences from control (WT and Sicontrol) strains according to Student's t-test (*P <0.05, **P <0.01, n = 3).

Fig. 3. Key NOESY correlations for compounds 1–10 in Lanostane-type triterpenoids from the mycelial mat of Ganoderma lucidum and their hepatoprotective activities

Fig. 3. Key NOESY correlations for compounds 1–10.

Fig. 2. Key 1H–1H in Lanostane-type triterpenoids from the mycelial mat of Ganoderma lucidum and their hepatoprotective activities

Fig. 2. Key 1H–1H COSY and HMBC correlations of compounds 1–10.

Fig. 1 in Lanostane-type triterpenoids from the mycelial mat of Ganoderma lucidum and their hepatoprotective activities

Fig. 1. Structures of compounds 1–31.

Fig. 3 in Lanostane triterpenoids with anti-inflammatory activities from Ganoderma lucidum

Fig. 3. Key NOESY correlations of compounds 1–5, 7 and 8.

Fig. 2. Key HMBC and 1H–1H in Lanostane triterpenoids with anti-inflammatory activities from Ganoderma lucidum

Fig. 2. Key HMBC and 1H–1H COSY correlations of compounds 1–8.

Fig. 1 in Lanostane triterpenoids with anti-inflammatory activities from Ganoderma lucidum

Fig. 1. Structures of compounds 1–15.

Fig. 4. Single-crystal X in Lanostane triterpenoids with anti-inflammatory activities from Ganoderma lucidum

Fig. 4. Single-crystal X-ray structure of 5.