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Effects of PQQ treatment on mitochondrial damage induced by ENR exposure in IEC‐6 cells. (A) Experimental design diagram. (B) Network diagram depicting mitochondrial‐related genes and associated biological pathways. (C–M) Differentially expressed genes related to mitochondrial function. (N–O) Protein levels of <t>Tomm20</t> measured by Western blot analysis. (P) OCR was recorded at baseline and after the sequential injection of oligomycin, FCCP, and a mixture of rotenone and antimycin A. (Q–T) Quantitative analysis of mitochondrial respiration parameters: Basal respiration (Q), ATP‐linked respiration (R), proton leak (S), and maximal respiration (T). Statistical significance among the Control, ENR, and ENR + PQQ groups was assessed using one‐way ANOVA followed by Tukey's multiple‐comparisons test. * p < 0.05, ** p < 0.01, *** p < 0.001.
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Effects of PQQ treatment on mitochondrial damage induced by ENR exposure in IEC‐6 cells. (A) Experimental design diagram. (B) Network diagram depicting mitochondrial‐related genes and associated biological pathways. (C–M) Differentially expressed genes related to mitochondrial function. (N–O) Protein levels of <t>Tomm20</t> measured by Western blot analysis. (P) OCR was recorded at baseline and after the sequential injection of oligomycin, FCCP, and a mixture of rotenone and antimycin A. (Q–T) Quantitative analysis of mitochondrial respiration parameters: Basal respiration (Q), ATP‐linked respiration (R), proton leak (S), and maximal respiration (T). Statistical significance among the Control, ENR, and ENR + PQQ groups was assessed using one‐way ANOVA followed by Tukey's multiple‐comparisons test. * p < 0.05, ** p < 0.01, *** p < 0.001.
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Effects of PQQ treatment on mitochondrial damage induced by ENR exposure in IEC‐6 cells. (A) Experimental design diagram. (B) Network diagram depicting mitochondrial‐related genes and associated biological pathways. (C–M) Differentially expressed genes related to mitochondrial function. (N–O) Protein levels of <t>Tomm20</t> measured by Western blot analysis. (P) OCR was recorded at baseline and after the sequential injection of oligomycin, FCCP, and a mixture of rotenone and antimycin A. (Q–T) Quantitative analysis of mitochondrial respiration parameters: Basal respiration (Q), ATP‐linked respiration (R), proton leak (S), and maximal respiration (T). Statistical significance among the Control, ENR, and ENR + PQQ groups was assessed using one‐way ANOVA followed by Tukey's multiple‐comparisons test. * p < 0.05, ** p < 0.01, *** p < 0.001.
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Effects of PQQ treatment on mitochondrial damage induced by ENR exposure in IEC‐6 cells. (A) Experimental design diagram. (B) Network diagram depicting mitochondrial‐related genes and associated biological pathways. (C–M) Differentially expressed genes related to mitochondrial function. (N–O) Protein levels of <t>Tomm20</t> measured by Western blot analysis. (P) OCR was recorded at baseline and after the sequential injection of oligomycin, FCCP, and a mixture of rotenone and antimycin A. (Q–T) Quantitative analysis of mitochondrial respiration parameters: Basal respiration (Q), ATP‐linked respiration (R), proton leak (S), and maximal respiration (T). Statistical significance among the Control, ENR, and ENR + PQQ groups was assessed using one‐way ANOVA followed by Tukey's multiple‐comparisons test. * p < 0.05, ** p < 0.01, *** p < 0.001.
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Image Search Results


Effects of PQQ treatment on mitochondrial damage induced by ENR exposure in IEC‐6 cells. (A) Experimental design diagram. (B) Network diagram depicting mitochondrial‐related genes and associated biological pathways. (C–M) Differentially expressed genes related to mitochondrial function. (N–O) Protein levels of Tomm20 measured by Western blot analysis. (P) OCR was recorded at baseline and after the sequential injection of oligomycin, FCCP, and a mixture of rotenone and antimycin A. (Q–T) Quantitative analysis of mitochondrial respiration parameters: Basal respiration (Q), ATP‐linked respiration (R), proton leak (S), and maximal respiration (T). Statistical significance among the Control, ENR, and ENR + PQQ groups was assessed using one‐way ANOVA followed by Tukey's multiple‐comparisons test. * p < 0.05, ** p < 0.01, *** p < 0.001.

Journal: Aging Cell

Article Title: Environmental Enrofloxacin Exposure as a Modifiable Driver of Mitochondria‐Mediated Intestinal Aging and Barrier Dysfunction

doi: 10.1111/acel.70526

Figure Lengend Snippet: Effects of PQQ treatment on mitochondrial damage induced by ENR exposure in IEC‐6 cells. (A) Experimental design diagram. (B) Network diagram depicting mitochondrial‐related genes and associated biological pathways. (C–M) Differentially expressed genes related to mitochondrial function. (N–O) Protein levels of Tomm20 measured by Western blot analysis. (P) OCR was recorded at baseline and after the sequential injection of oligomycin, FCCP, and a mixture of rotenone and antimycin A. (Q–T) Quantitative analysis of mitochondrial respiration parameters: Basal respiration (Q), ATP‐linked respiration (R), proton leak (S), and maximal respiration (T). Statistical significance among the Control, ENR, and ENR + PQQ groups was assessed using one‐way ANOVA followed by Tukey's multiple‐comparisons test. * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: Intestinal tissues were fixed (4% paraformaldehyde, 15 min), blocked (10% goat serum albumin, 0.4% Triton X‐100), and incubated with primary antibodies from Servicebio: Cdkn1a (GB11153, 1:300), Cdkn2a ( GB151143 , 1:300), Tomm20 ( GB151481 , 1:1000), Grp75 ( GB112273 , 1:650), Cox5a ( GB111676 , 1:500), Hsp60 ( GB112464 , 1:800), Cox4 (GB11250, 1:200), CD3 (GB13014, 1:100), Mucin‐2 (GB11344, 1:500), Occludin ( GB111401 , 1:750), Zo‐1 ( GB115686 , 1:1000), and Claudin‐1 ( GB112543 , 1:1000).

Techniques: Western Blot, Injection, Control

Effects of PQQ treatment on mitochondrial function, inflammation, and hypoxia levels in the intestine following ENR exposure. Experimental design diagram (A). Representative immunofluorescence images of mitochondrial function‐related proteins (Hsp60, Cox4, Tomm20, Grp75, Cox5a) and quantification (B–I). Representative immunofluorescence images of CD3 and quantification (J–K). Representative immunofluorescence images of hypoxia markers and quantification (L, M). Data are presented as the mean ± standard error of the mean. Statistical significance among the Control, ENR, and ENR + PQQ groups was assessed using one‐way ANOVA followed by Tukey's multiple‐comparisons test. * p < 0.05, ** p < 0.01, *** p < 0.001.

Journal: Aging Cell

Article Title: Environmental Enrofloxacin Exposure as a Modifiable Driver of Mitochondria‐Mediated Intestinal Aging and Barrier Dysfunction

doi: 10.1111/acel.70526

Figure Lengend Snippet: Effects of PQQ treatment on mitochondrial function, inflammation, and hypoxia levels in the intestine following ENR exposure. Experimental design diagram (A). Representative immunofluorescence images of mitochondrial function‐related proteins (Hsp60, Cox4, Tomm20, Grp75, Cox5a) and quantification (B–I). Representative immunofluorescence images of CD3 and quantification (J–K). Representative immunofluorescence images of hypoxia markers and quantification (L, M). Data are presented as the mean ± standard error of the mean. Statistical significance among the Control, ENR, and ENR + PQQ groups was assessed using one‐way ANOVA followed by Tukey's multiple‐comparisons test. * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: Intestinal tissues were fixed (4% paraformaldehyde, 15 min), blocked (10% goat serum albumin, 0.4% Triton X‐100), and incubated with primary antibodies from Servicebio: Cdkn1a (GB11153, 1:300), Cdkn2a ( GB151143 , 1:300), Tomm20 ( GB151481 , 1:1000), Grp75 ( GB112273 , 1:650), Cox5a ( GB111676 , 1:500), Hsp60 ( GB112464 , 1:800), Cox4 (GB11250, 1:200), CD3 (GB13014, 1:100), Mucin‐2 (GB11344, 1:500), Occludin ( GB111401 , 1:750), Zo‐1 ( GB115686 , 1:1000), and Claudin‐1 ( GB112543 , 1:1000).

Techniques: Immunofluorescence, Control