Zerumbone turns on two important antioxidant genes (HO-1 and γ-GCLC) in skin cells, helping them fight off damage—HO-1 stays turned on for a full day.

Scientific Claim

Zerumbone at 2–8 μM upregulates expression of the antioxidant enzymes HO-1 and γ-GCLC in human skin fibroblasts via Nrf2-dependent transcriptional activation, with HO-1 showing sustained induction up to 24 hours.

Original Statement

“ZER treatment significantly upregulated the expression of HO-1 protein levels from 4 to 24 h time points, whereas γ-GCLC levels were upregulated up to 4 h time point and then gradually decreased till 24 h (Figures 5(c) and 5(d)).”

From study:Zerumbone Exhibits Antiphotoaging and Dermatoprotective Properties in Ultraviolet A-Irradiated Human Skin Fibroblast Cells via the Activation of Nrf2/ARE Defensive Pathway

Evidence Quality Assessment

Claim Status

appropriately stated

Study Design Support

Design supports claim

Appropriate Language Strength

definitive

Can make definitive causal claims

Assessment Explanation

Protein expression was directly measured over time with statistical significance; the claim accurately reflects the observed kinetics without extrapolation.

Evidence from Studies

Supporting (1)

Zerumbone Exhibits Antiphotoaging and Dermatoprotective Properties in Ultraviolet A-Irradiated Human Skin Fibroblast Cells via the Activation of Nrf2/ARE Defensive Pathway

Cross-Sectional Study

In Vitro

The study shows that zerumbone, a natural compound, turns on a cellular defense system (Nrf2) that boosts protective enzymes like HO-1 and γ-GCLC in skin cells, helping them fight damage from sunlight — exactly what the claim says.

Contradicting (0)

No contradicting evidence found

Source Study

Zerumbone Exhibits Antiphotoaging and Dermatoprotective Properties in Ultraviolet A-Irradiated Human Skin Fibroblast Cells via the Activation of Nrf2/ARE Defensive Pathway

Score: 5

DOI: 10.1155/2019/4098674

Similar Assertions

When scientists turned off the Nrf2 gene, zerumbone lost its ability to protect skin cells from UVA damage—proving Nrf2 is necessary for its effect.

83%

Zerumbone helps a master switch (Nrf2) move into the nucleus of skin cells, turning on protective genes—this happens within 30 minutes to 4 hours.

82%

Zerumbone turns up the volume on a genetic switch (ARE) that controls antioxidant genes—more zerumbone means louder activation.

82%

Zerumbone slightly increases harmful molecules (ROS) in skin cells before UVA hits—this small rise is actually needed to activate the cell’s defense system.

80%

Zerumbone doesn’t just use one path to activate the cell’s defense system—it uses at least seven different signaling routes to turn on protective genes.

78%