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Fig. 1 Andrographolide protected mice from radiation-induced lung injury. Mice were exposed to 18 Gy irradiation and then treated with the indicated doses of Andrographolide for 4 weeks after irradiation. a Representative images of mice at 8 weeks post-ir
Figure 2. Fig. 1 Andrographolide protected mice from radiation-induced lung injury. Mice were exposed to 18 Gy irradiation and then treated with the indicated doses of Andrographolide for 4 weeks after irradiation. a Representative images of mice at 8 weeks post-irradiation. b Kaplan–Meier survival analysis of mice in different groups, n 12 per group. c Representative images of H&E staining of lung tissues from each group. Alveolar hemorrhage and the thickness of the alveolar walls were indicated by arrows. Scale bar, 50 μm. d Semi-quantitative histological analysis of lung tissues of five fields per mouse in every group. e Lung coefficient of mice in each group. The results are shown as the mean ± S.E.M., n = 6 mice per group. *P < 0.05 vs the IR group.

Deskripsi

Mice exposed to 18 Gy irradiation and treated with varying doses of andrographolide for 4 weeks showed dose-dependent protection from radiation-induced lung injury. Representative images and quantitative data indicate that andrographolide significantly attenuated lung tissue damage.

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Histological analysis of lung tissue from irradiated mice reveals the extent of inflammatory cell infiltration and fibrosis. Andrographolide treatment appears to reduce these pathological changes in a dose-dependent manner.

Figure 3

Histological analysis of lung tissue from irradiated mice reveals the extent of inflammatory cell infiltration and fibrosis. Andrographolide treatment appears to reduce these pathological changes in a dose-dependent manner.

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Inflammatory cytokine levels in lung tissue were measured following radiation exposure and andrographolide treatment. The data suggest that andrographolide suppresses pro-inflammatory mediator release in irradiated lung tissue.

Figure 4

Inflammatory cytokine levels in lung tissue were measured following radiation exposure and andrographolide treatment. The data suggest that andrographolide suppresses pro-inflammatory mediator release in irradiated lung tissue.

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AIM2 inflammasome activation and caspase-1-mediated pyroptosis play key roles in radiation-induced lung inflammation. This figure presents protein expression data showing andrographolide's inhibitory effects on the AIM2 inflammasome pathway.

Figure 5

AIM2 inflammasome activation and caspase-1-mediated pyroptosis play key roles in radiation-induced lung inflammation. This figure presents protein expression data showing andrographolide's inhibitory effects on the AIM2 inflammasome pathway.

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Gasdermin D cleavage is a downstream event in pyroptotic cell death triggered by radiation. Western blot analysis demonstrates that andrographolide reduces Gasdermin D processing in macrophages exposed to radiation.

Figure 6

Gasdermin D cleavage is a downstream event in pyroptotic cell death triggered by radiation. Western blot analysis demonstrates that andrographolide reduces Gasdermin D processing in macrophages exposed to radiation.

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Immunofluorescence or protein analysis reveals that andrographolide prevents AIM2 from binding cytoplasmic DNA and forming active inflammasome complexes. These findings indicate a specific molecular target for andrographolide's protective mechanism.

Figure 7

Immunofluorescence or protein analysis reveals that andrographolide prevents AIM2 from binding cytoplasmic DNA and forming active inflammasome complexes. These findings indicate a specific molecular target for andrographolide's protective mechanism.

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Andrographolide ameliorates radiation-induced lung injury by inhibiting Caspase-1-mediated Gasdermin D-dependent pyroptosis in macrophages. This schematic illustrates how the compound prevents AIM2 from translocating into the nucleus, thereby blocking inflammasome assembly and downstream inflammatory cascades.

Figure 8

Andrographolide ameliorates radiation-induced lung injury by inhibiting Caspase-1-mediated Gasdermin D-dependent pyroptosis in macrophages. This schematic illustrates how the compound prevents AIM2 from translocating into the nucleus, thereby blocking inflammasome assembly and downstream inflammatory cascades.

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Figure 2

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Source Paper

Inhibition of AIM2 inflammasome-mediated pyroptosis by Andrographolide contributes to amelioration of radiation-induced lung inflammation and fibrosis.

Cell death & disease (2019)

PMID: 31862870

DOI: 10.1038/s41419-019-2195-8

Cite This Figure

![Figure 2: Mice exposed to 18 Gy irradiation and treated with varying doses of andrographolide for 4 weeks showed dose-dependent protection from radiation-induced lung injury. Representative images and quantitative data indicate that andrographolide significantly attenuated lung tissue damage.](https://pdfs.citedhealth.com/figures/31862870/150.png)

> Source: Jian Gao et al. "Inhibition of AIM2 inflammasome-mediated pyroptosis by Andrographolide contribut." *Cell death & disease*, 2019. PMID: [31862870](https://pubmed.ncbi.nlm.nih.gov/31862870/)
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  <img src="https://pdfs.citedhealth.com/figures/31862870/150.png" alt="Mice exposed to 18 Gy irradiation and treated with varying doses of andrographolide for 4 weeks showed dose-dependent protection from radiation-induced lung injury. Representative images and quantitative data indicate that andrographolide significantly attenuated lung tissue damage." />
  <figcaption>Figure 2. Mice exposed to 18 Gy irradiation and treated with varying doses of andrographolide for 4 weeks showed dose-dependent protection from radiation-induced lung injury. Representative images and quantitative data indicate that andrographolide significantly attenuated lung tissue damage.<br>  Source: Jian Gao et al. "Inhibition of AIM2 inflammasome-mediated pyroptosis by Andrographolide contribut." <em>Cell death & disease</em>, 2019. PMID: <a href="https://pubmed.ncbi.nlm.nih.gov/31862870/">31862870</a></figcaption>
</figure>

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