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Study · In vitro (cells) · 2015

9 results

Mitochondrion-Targeted Peptide SS-31 Inhibited Oxidized Low-Density Lipoproteins-Induced Foam Cell Formation through both ROS Scavenging and Inhibition of Cholesterol Influx in RAW264.7 Cells.

Hao S, Ji J, Zhao H, Shang L, Wu J, Li H, Qiao T, Li K

Molecules (Basel, Switzerland)1 Dec 2015Cited by 36 (Europe PMC)

Summary

Foam cell formation as a result of imbalance of modified cholesterol influx and efflux by macrophages is a key to the occurrence and development of atherosclerosis. Oxidative stress is thought to be involved in the pathogenesis of atherosclerosis. SS-31 is a member of the Szeto-Schiller (SS) peptides shown to specifically target the inner mitochondrial membrane to scavenge reactive oxygen species. In this study, we investigated whether SS-31 may provide protective effect on macrophage from foam cell formation in RAW264.7 cells. The results showed that SS-31 inhibited oxidized low-density lipoproteins (ox-LDL)-induced foam cell formation and cholesterol accumulation, demonstrated by intracellular oil red O staining and measurement of cholesterol content. The mechanism was revealed that SS-31 did not only significantly attenuated ox-LDL-induced generation of reactive oxygen species (ROS) and increased the activities of superoxide dismutases, but also dose-dependently inhibited the expression of CD36 and LOX-1, two scavenger receptors of ox-LDL, while the expression of ATP-binding cassette A1 and G1, playing a pivotal role in cholesterol efflux, was not affected. As a result, SS-31 decreased pro-inflammatory cytokines such as interleukin 6 and tumor necrosis factor alpha, suggesting the prevention of inflammatory responses. In conclusion, our results demonstrate that SS-31 provides a beneficial effect on macrophages from foam cell formation, likely, through both ROS scavenging and inhibition of cholesterol influx. Therefore, SS-31 may potentially be of therapeutic relevance in prevention of human atherogenesis.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study9

9 results from studies that gave the peptide. No result from this study comes from people.

  1. 01LabIn vitro (cells)Efficacy outcome

    In RAW264.7 macrophages, SS‑31 inhibited ox-LDL-induced foam cell formation.

    In plain wordsIn lab-grown macrophages, SS‑31 reduced the formation of fat-laden foam cells triggered by oxidized LDL.

    Outcome
    Decreaseox-LDL-induced foam cell formation
    Study

    n: not reported in source

    RAW264.7 macrophages with ox-LDL
    Comparator
    ox-LDL without SS-31
    Outcome group
    Lipids · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    The results showed that SS-31 inhibited oxidized low-density lipoproteins (ox-LDL)-induced foam cell formation and cholesterol accumulation, demonstrated by intracellular oil red O staining and measurement of cholesterol content.
    1 context sentence
    Summary · context
    In this study, we investigated whether SS-31 may provide protective effect on macrophage from foam cell formation in RAW264.7 cells.
  2. 02LabIn vitro (cells)Efficacy outcome

    In RAW264.7 macrophages, SS‑31 inhibited ox-LDL-induced cholesterol accumulation.

    In plain wordsIn lab-grown macrophages, SS‑31 reduced cholesterol build-up caused by oxidized LDL.

    Outcome
    DecreaseCholesterol accumulation
    Study

    n: not reported in source

    RAW264.7 macrophages with ox-LDL
    Comparator
    ox-LDL without SS-31
    Outcome group
    Lipids · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    The results showed that SS-31 inhibited oxidized low-density lipoproteins (ox-LDL)-induced foam cell formation and cholesterol accumulation, demonstrated by intracellular oil red O staining and measurement of cholesterol content.
    1 context sentence
    Summary · context
    In this study, we investigated whether SS-31 may provide protective effect on macrophage from foam cell formation in RAW264.7 cells.
  3. 03LabIn vitro (cells)Mechanism

    In RAW264.7 macrophages, SS‑31 significantly attenuated ox-LDL-induced generation of reactive oxygen species.

    In plain wordsIn lab-grown macrophages, SS‑31 lowered the reactive oxygen species made after oxidized LDL exposure.

    Outcome
    Decreaseox-LDL-induced ROS generation
    Study

    n: not reported in source

    RAW264.7 macrophages with ox-LDL
    Comparator
    ox-LDL without SS-31
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    significantly attenuated ox-LDL-induced generation of reactive oxygen species (ROS)
    1 context sentence
    Summary · context
    In this study, we investigated whether SS-31 may provide protective effect on macrophage from foam cell formation in RAW264.7 cells.
  4. 04LabIn vitro (cells)Mechanism

    In RAW264.7 macrophages, SS‑31 increased the activities of superoxide dismutases.

    In plain wordsIn lab-grown macrophages, SS‑31 raised the activity of antioxidant enzymes called superoxide dismutases.

    Outcome
    IncreaseSuperoxide dismutase activity
    Study

    n: not reported in source

    RAW264.7 macrophages with ox-LDL
    Comparator
    ox-LDL without SS-31
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    increased the activities of superoxide dismutases
    1 context sentence
    Summary · context
    In this study, we investigated whether SS-31 may provide protective effect on macrophage from foam cell formation in RAW264.7 cells.
  5. 05LabIn vitro (cells)Mechanism

    In RAW264.7 macrophages, SS‑31 dose-dependently inhibited the expression of the ox-LDL scavenger receptor CD36.

    In plain wordsIn lab-grown macrophages, SS‑31 reduced, in a dose-dependent way, a receptor (CD36) that takes up oxidized LDL.

    Outcome
    DecreaseCD36 expression
    Study

    n: not reported in source

    RAW264.7 macrophages with ox-LDL
    Comparator
    ox-LDL without SS-31
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    dose-dependently inhibited the expression of CD36 and LOX-1
    1 context sentence
    Summary · context
    In this study, we investigated whether SS-31 may provide protective effect on macrophage from foam cell formation in RAW264.7 cells.
  6. 06LabIn vitro (cells)Mechanism

    In RAW264.7 macrophages, SS‑31 dose-dependently inhibited the expression of the ox-LDL scavenger receptor LOX-1.

    In plain wordsIn lab-grown macrophages, SS‑31 reduced, in a dose-dependent way, a receptor (LOX-1) that takes up oxidized LDL.

    Outcome
    DecreaseLOX-1 expression
    Study

    n: not reported in source

    RAW264.7 macrophages with ox-LDL
    Comparator
    ox-LDL without SS-31
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    dose-dependently inhibited the expression of CD36 and LOX-1
    1 context sentence
    Summary · context
    In this study, we investigated whether SS-31 may provide protective effect on macrophage from foam cell formation in RAW264.7 cells.
  7. 07LabIn vitro (cells)Mechanism

    In RAW264.7 macrophages, SS‑31 did not affect the expression of the cholesterol efflux transporters ABCA1 and ABCG1.

    In plain wordsIn lab-grown macrophages, SS‑31 did not change the cholesterol-export proteins ABCA1 and ABCG1.

    Outcome
    No significant changeABCA1 and ABCG1 expression
    Study

    n: not reported in source

    RAW264.7 macrophages with ox-LDL
    Comparator
    ox-LDL without SS-31
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    while the expression of ATP-binding cassette A1 and G1, playing a pivotal role in cholesterol efflux, was not affected.
    1 context sentence
    Summary · context
    In this study, we investigated whether SS-31 may provide protective effect on macrophage from foam cell formation in RAW264.7 cells.
  8. 08LabIn vitro (cells)Mechanism

    In RAW264.7 macrophages, SS‑31 decreased the pro-inflammatory cytokine interleukin 6.

    In plain wordsIn lab-grown macrophages, SS‑31 lowered the inflammation signal interleukin 6.

    Outcome
    DecreaseInterleukin 6
    Study

    n: not reported in source

    RAW264.7 macrophages with ox-LDL
    Comparator
    ox-LDL without SS-31
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    SS-31 decreased pro-inflammatory cytokines such as interleukin 6 and tumor necrosis factor alpha
    1 context sentence
    Summary · context
    In this study, we investigated whether SS-31 may provide protective effect on macrophage from foam cell formation in RAW264.7 cells.
  9. 09LabIn vitro (cells)Mechanism

    In RAW264.7 macrophages, SS‑31 decreased the pro-inflammatory cytokine tumor necrosis factor alpha.

    In plain wordsIn lab-grown macrophages, SS‑31 lowered the inflammation signal tumor necrosis factor alpha.

    Outcome
    DecreaseTumor necrosis factor alpha
    Study

    n: not reported in source

    RAW264.7 macrophages with ox-LDL
    Comparator
    ox-LDL without SS-31
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    SS-31 decreased pro-inflammatory cytokines such as interleukin 6 and tumor necrosis factor alpha
    1 context sentence
    Summary · context
    In this study, we investigated whether SS-31 may provide protective effect on macrophage from foam cell formation in RAW264.7 cells.

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

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  1. Version 2Current

    10 Oct 2026, 08:19 UTC

    Study results updated

  2. Version 1

    9 Oct 2026, 02:47 UTC

    First added · source update from Europe PMC

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