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Fig. 4 in Diterpenoid alkaloids from Delphinium forrestii var. viride and their anti-inflammation activity

Fig. 4. Effect of compounds 1–15 on LPS-induced production of NO. Dexamethasone (Dex) was used as the positive control.

Fig. 8. Forrestline F suppressed LPSinduced inflammatory activity through Nrf2 in Diterpenoid alkaloids from Delphinium forrestii var. viride and their anti-inflammation activity

Fig. 8. Forrestline F suppressed LPSinduced inflammatory activity through Nrf2 pathways and promoted the LPSinduced nuclear translocation of Nrf2. (A–B) The cells were exposed to forrestline F (5, 10, 20 μM) for 3 h and cultured with LPS for 24 h, except for the control group. The protein expression of Keap-1/Nrf2 pathway was determined by western blotting and the quantifications of protein expression were performed by Image J. (C) The inhibitory effect of forrestline F (20 μM) on the nuclear translocation of Nrf2 induced by LPS via confocal laser scanning microscopy, in conjunction with nuclear DAPI stain (scale bar: 50 μM). The values are presented as mean ± SD of three independent experiments, n = 3. ###p <0.001, vs. the control group; ***p <0.001, vs. LPS-stimulated group.

Fig. 5. Forrestline F in Diterpenoid alkaloids from Delphinium forrestii var. viride and their anti-inflammation activity

Fig. 5. Forrestline F reduced LPS-induced the pro-inflammatory cytokines release and the expression of iNOS and COX-2 in RAW 264.7 cells. (A)The chemical structure of forrestline F. (B) Cell viability rate of RAW264.7 cells treated with concentration gradient of forrestline F (0–100 μM) in the presence or absence of LPS (0.5 μg/mL) for 24 h. (C) The NO inhibition curve of forrestline F, with an IC50 of 9.57 ± 1.34 μM. (D–F) Effects of forrestline F on productions of inflammatory cytokines (IL-1β, TNF-α and IL-6) in LPS-activated RAW264.7 cells. (G–I) The protein expression of iNOS and COX-2 was determined by western blotting. The values are presented as mean ± SD of three independent experiments, n = 3. ###p <0.001, vs. the control group; **p <0.01, ***p <0.001, vs. LPS-stimulated group.

Fig. 7. Forrestline F in Diterpenoid alkaloids from Delphinium forrestii var. viride and their anti-inflammation activity

Fig. 7. Forrestline F decreased LPS-induced ROS generation and mitochondrial membrane potential loss. (A) Cells were cultured with LPS for 12 h after treated with forrestline F (5, 10 and 20 μM) for 3 h, except the control group and the group only treated with LPS. After cells were incubated with DCFH-DA (10 μM) for 20 min, images were acquired with a fluorescence microscope (scale bar: 200 μM). (B) The cells were processed in the same way as above, and collected to flow tube and monitored by the flow cytometry. (C) Statistical analysis of the fluorescence intensity of DCFH-DA. (D–E) For the measurement of MMP, JC-1 fluorescent dyes were loaded for 20 min and images were acquired with flow cytometry. The values are presented as mean SD of three independent experiments, n 3. ###p <0.001, vs. ± = the control group; **p <0.01, ***p <0.001, vs. LPS-stimulated group.

Fig. 6. Forrestline F in Diterpenoid alkaloids from Delphinium forrestii var. viride and their anti-inflammation activity

Fig. 6. Forrestline F reduced LPS-induced inflammatory activity through the NF-κB/MAPK pathways and blocked the LPS-induced nuclear translocation of NF-κB. (A–B) The cells were exposed to forrestline F (5, 10 and 20 μM) for 3 h and cultured with LPS for 24 h, except for the control group. The protein expression of NF-κB pathway was determined by western blotting and the quantification of protein expression was performed by Image J. (C) The inhibitory effect of forrestline F on the nuclear translocation of NF-κB p65 induced by LPS via confocal laser scanning microscopy, in conjunction with nuclear DAPI stain (scale bar: 50 μM). (D–E) Protein expression of MAPK pathway, including p-ERK1/2 and p-p38 and p-JNK1/2, was measured by western blotting. The values are presented as mean ± SD of three independent experiments, n 3 ###p <0.001, vs. the control group; ***p <0.001, vs. LPS-stimulated group.

closedIPD-NOFeb 2026View details →

The Açaí Berry COVID-19 Anti-Inflammation Trial

ClinicalTrials.gov study NCT04404218. IPD Sharing: NO. Countries: 2. Publications: 5.

closedIPD-NOFeb 2026View details →

Optimizing Ultrasound-induced Anti-inflammation in Human Subjects

ClinicalTrials.gov study NCT05685108. IPD Sharing: NO. Countries: 1. Publications: 4.

restrictedIPD-UNDECIDEDFeb 2026View details →

The Clinical Efficacy of Non-steroidal Anti-inflammation Drugs in Patients With Benign Prostatic Hyperplasia

ClinicalTrials.gov study NCT00687388. IPD Sharing: Not stated. Countries: 1. Publications: 10.

closedIPD-NOFeb 2026View details →

Maintenance at Initial Treatment With Sequential Anti-Inflammation Reliever Therapy

ClinicalTrials.gov study NCT06568445. IPD Sharing: NO. Countries: 1. Publications: 16.

Fig. 4 in Callnudoids A-H: Highly modified labdane diterpenoids with anti-inflammation from the leaves of Callicarpa nudiflora

Fig. 4. Base hydrolysis reaction of compound 3.

Fig. 3 in Callnudoids A-H: Highly modified labdane diterpenoids with anti-inflammation from the leaves of Callicarpa nudiflora

Fig. 3. NOESY correlations of compounds 1, 4, 5, and 9.

Fig. 1 in Callnudoids A-H: Highly modified labdane diterpenoids with anti-inflammation from the leaves of Callicarpa nudiflora

Fig. 1. Structures of compounds 1–10.

Fig. 2. 1H–1H in Callnudoids A-H: Highly modified labdane diterpenoids with anti-inflammation from the leaves of Callicarpa nudiflora

Fig. 2. 1H–1H COSY and key HMBC correlations of compounds 1, 3–5, 7, and 9.

Fig. 5 in Callnudoids A-H: Highly modified labdane diterpenoids with anti-inflammation from the leaves of Callicarpa nudiflora

Fig. 5. Experimental and calculated ECD spectra of compound 4 (in MeOH).

Fig. 6 in Callnudoids A-H: Highly modified labdane diterpenoids with anti-inflammation from the leaves of Callicarpa nudiflora

Fig. 6. ORTEP drawing of compound 5.

Fig. 7 in Callnudoids A-H: Highly modified labdane diterpenoids with anti-inflammation from the leaves of Callicarpa nudiflora

Fig. 7. Plausible biosynthetic pathway for the formation of 1, 2, 4, and 5.

Fig. 1 in Diterpenoid alkaloids from Delphinium forrestii var. viride and their anti-inflammation activity

Fig. 1. Structures of 1–15 from D. forrestii var. viride.

Fig. 3 in Diterpenoid alkaloids from Delphinium forrestii var. viride and their anti-inflammation activity

Fig. 3. Selected NOESY correlations of compounds 1–6.