Figures & data
Figure 1. Production of gastric lesions and expression of HSPs in wild-type and HSF1-null mice. Wild-type (WT) and HSF1-null mice (HSF1-KO) were orally administered the indicated doses of ethanol (A, C) or hydrochloric acid (B). After 4 h, the stomach was removed and scored for haemorrhagic damage. Values are mean ± SEM (n = 4–6). *P < 0.05 (A, B). After 4 h, the gastric mucosa was removed, and protein extracts were prepared and analysed by immunoblotting with an antibody against Hsp25, Hsp60, Hsp70, Hsp90, or actin (C). This figures was published previously and is reprinted here with permission of the journal Citation[21].
![Figure 1. Production of gastric lesions and expression of HSPs in wild-type and HSF1-null mice. Wild-type (WT) and HSF1-null mice (HSF1-KO) were orally administered the indicated doses of ethanol (A, C) or hydrochloric acid (B). After 4 h, the stomach was removed and scored for haemorrhagic damage. Values are mean ± SEM (n = 4–6). *P < 0.05 (A, B). After 4 h, the gastric mucosa was removed, and protein extracts were prepared and analysed by immunoblotting with an antibody against Hsp25, Hsp60, Hsp70, Hsp90, or actin (C). This figures was published previously and is reprinted here with permission of the journal Citation[21].](/cms/asset/c9605665-d56b-41e4-9d5b-99ebdd0b40c8/ihyt_a_421510_f0001_b.gif)
Figure 2. Effect of ethanol and/or GGA on expression of Hsp70 and production of gastric lesions. Wild-type (WT) (A, C) and HSF1-null (HSF1-KO) (B, C) mice were orally pre-administered 200 mg/kg GGA (10 mL/kg as emulsion with 5% gum arabic), 1 h after which they were orally administered with the indicated doses of ethanol. After 4 h, sections of gastric tissues were prepared and subjected to histological examination (H&E) and immunohistochemical analysis with an antibody against Hsp70 (A, B). After 4 h, the stomach was removed and scored for haemorrhagic damage. Values are mean ± SEM (n = 3–6). *P < 0.05. n.s., not significant (C). This figure was published previously and is reprinted here with permission of the journal Citation[21].
![Figure 2. Effect of ethanol and/or GGA on expression of Hsp70 and production of gastric lesions. Wild-type (WT) (A, C) and HSF1-null (HSF1-KO) (B, C) mice were orally pre-administered 200 mg/kg GGA (10 mL/kg as emulsion with 5% gum arabic), 1 h after which they were orally administered with the indicated doses of ethanol. After 4 h, sections of gastric tissues were prepared and subjected to histological examination (H&E) and immunohistochemical analysis with an antibody against Hsp70 (A, B). After 4 h, the stomach was removed and scored for haemorrhagic damage. Values are mean ± SEM (n = 3–6). *P < 0.05. n.s., not significant (C). This figure was published previously and is reprinted here with permission of the journal Citation[21].](/cms/asset/d1ddb869-3bf8-42c1-be8f-4a62a94e48ed/ihyt_a_421510_f0002_b.gif)
Figure 3. The mRNA expression of various genes and levels of cell death in colonic mucosa. Transgenic mice expressing Hsp70 (Hsp70 Tg) and wild-type mice (WT) were treated with or without 3% DSS for 7 days (A, B). Relative mRNA expression of each gene in colonic tissues was monitored and expressed. Values are mean ± SEM (n = 3–6). **P < 0.01; *P < 0.05 (A). Sections of colonic tissues were prepared and subjected to TUNEL assay and DAPI staining (B). This figure was published previously and is reprinted here with permission of the journal Citation[23].
![Figure 3. The mRNA expression of various genes and levels of cell death in colonic mucosa. Transgenic mice expressing Hsp70 (Hsp70 Tg) and wild-type mice (WT) were treated with or without 3% DSS for 7 days (A, B). Relative mRNA expression of each gene in colonic tissues was monitored and expressed. Values are mean ± SEM (n = 3–6). **P < 0.01; *P < 0.05 (A). Sections of colonic tissues were prepared and subjected to TUNEL assay and DAPI staining (B). This figure was published previously and is reprinted here with permission of the journal Citation[23].](/cms/asset/55ea3b47-0f42-44cf-a330-5d1749c7eb3c/ihyt_a_421510_f0003_b.gif)
Figure 4. The proposed mechanism for protective role of HSF1 and Hsp70 against gastric ulcer (A) and IBD (B).
