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Hesperetin prevents selenite-induced cataract in rats.

Nakazawa Y, Oka M, Bando M, Takehana M - Mol. Vis. (2015)

Bottom Line: Lenses were observed with slit-lamp microscopy, and filensin degradation and the decreased glutathione (GSH) and ascorbic acid levels in the lens were measured on day 6.Expression of the 94 kDa and 50 kDa forms of filensin was significantly decreased in the lenses in the G3 group compared with those in the G1 and G2 groups.In the G3 group lenses, the GSH and ascorbic acid levels were lower than in the control group but were normalized in the G4 group lenses.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular Function and Physiology, Faculty of Pharmacy, Keio University ; Division of Hygienic Chemistry, Faculty of Pharmacy, Keio University.

ABSTRACT

Purpose: This study investigated the ability of hesperetin, a natural flavonoid, to prevent selenite-induced cataracts in a rat model.

Methods: Animals were divided into four treatment groups: G1 (control group), G2 (hesperetin-treated group), G3 (selenite-induced cataract group), and G4 (hesperetin-treated selenite cataract group). Animals in the G1 and G3 groups were injected with vehicle alone, while those in the G2 and G4 groups received a subcutaneous injection of hesperetin (0.4 μg/g bodyweight on days 0, 1, and 2, corresponding to P13, P14, and P15). Sodium selenite (20 μmol/g bodyweight given 4 h after the hesperetin injection on day 0) was administered to rats in the G3 and G4 groups to induce cataract formation. Lenses were observed with slit-lamp microscopy, and filensin degradation and the decreased glutathione (GSH) and ascorbic acid levels in the lens were measured on day 6.

Results: Lenses in the G3 group showed mature central opacity, while some lenses in the G4 group lacked central opacity and had lower-grade cataracts. All lenses in the G1 and G2 groups were transparent. Expression of the 94 kDa and 50 kDa forms of filensin was significantly decreased in the lenses in the G3 group compared with those in the G1 and G2 groups. Interestingly, these forms of filensin rescued the rat lenses in the G4 group. In the G3 group lenses, the GSH and ascorbic acid levels were lower than in the control group but were normalized in the G4 group lenses.

Conclusions: The results suggest that hesperetin can prevent selenite-induced cataract formation.

No MeSH data available.


Related in: MedlinePlus

Degradation of filensin. Western blot analysis with an anti-filensin antibody. A: The 94 kDa form of filensin is processed into the 50 kDa and 38 kDa forms in vivo (arrow). B: Western blot analysis with anti-β-actin antibody as an internal control. Lane 1: control group (G1). Lane 2: hesperetin-treated group (G2). Lane 3: selenite-treated group (G3). Lane 4: selenite and hesperetin-treated group (G4). M shows the molecular weight standards. C: The respective bar diagrams show the band intensity (densitometric value) of the 94 kDa (black bar), 50 kDa (gray bar), and 38 kDa (white bar) forms of filensin levels relative to the levels in the control G1 group. All bar diagrams are expressed as the mean ± SD, and statistical analysis was determined using the unpaired Student t-test. *p<0.05 versus control (G1 group) and †p<0.05 versus rats with selenite-induced cataracts without hesperetin treatment (G3 group; n = 9 in each group).
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f2: Degradation of filensin. Western blot analysis with an anti-filensin antibody. A: The 94 kDa form of filensin is processed into the 50 kDa and 38 kDa forms in vivo (arrow). B: Western blot analysis with anti-β-actin antibody as an internal control. Lane 1: control group (G1). Lane 2: hesperetin-treated group (G2). Lane 3: selenite-treated group (G3). Lane 4: selenite and hesperetin-treated group (G4). M shows the molecular weight standards. C: The respective bar diagrams show the band intensity (densitometric value) of the 94 kDa (black bar), 50 kDa (gray bar), and 38 kDa (white bar) forms of filensin levels relative to the levels in the control G1 group. All bar diagrams are expressed as the mean ± SD, and statistical analysis was determined using the unpaired Student t-test. *p<0.05 versus control (G1 group) and †p<0.05 versus rats with selenite-induced cataracts without hesperetin treatment (G3 group; n = 9 in each group).

Mentions: The degradation of filensin in selenite-induced cataract lenses was investigated with western blot analysis. The lenses from rats in the G1 and G2 groups contained the same proportions of the 94 kDa, 50 kDa, and 38 kDa forms of filensin (Figure 2, lanes 1 and 2). The 94 kDa and 50 kDa forms of filensin were significantly less abundant in lenses from the G3 group than in lenses from the G1 and G2 groups (Figure 2, lane 3). However, the intensities of the 94 kDa and 50 kDa form of filensin in lenses were rescued with the hesperetin treatment with selenite administered to rats (Figure 2, lane 4). The protein expression of β-actin was detected as an internal control of all groups (Figure 2B). The 94, 50, and 38 kDa forms of filensin normalized for β-actin were assessed using densitometry, and data are depicted graphically in Figure 3C. The 94 kDa and 50 kDa forms of filensin were significantly decreased in the G3 group compared to the G1 and G2 groups, and hesperetin treatment for rat cataract (the G4 group) inhibited the protein loss observed in the selenite-induced rat cataracts (the G3 group). Administration of hesperetin and/or selenite did not affect the 38 kDa form of filensin.


Hesperetin prevents selenite-induced cataract in rats.

Nakazawa Y, Oka M, Bando M, Takehana M - Mol. Vis. (2015)

Degradation of filensin. Western blot analysis with an anti-filensin antibody. A: The 94 kDa form of filensin is processed into the 50 kDa and 38 kDa forms in vivo (arrow). B: Western blot analysis with anti-β-actin antibody as an internal control. Lane 1: control group (G1). Lane 2: hesperetin-treated group (G2). Lane 3: selenite-treated group (G3). Lane 4: selenite and hesperetin-treated group (G4). M shows the molecular weight standards. C: The respective bar diagrams show the band intensity (densitometric value) of the 94 kDa (black bar), 50 kDa (gray bar), and 38 kDa (white bar) forms of filensin levels relative to the levels in the control G1 group. All bar diagrams are expressed as the mean ± SD, and statistical analysis was determined using the unpaired Student t-test. *p<0.05 versus control (G1 group) and †p<0.05 versus rats with selenite-induced cataracts without hesperetin treatment (G3 group; n = 9 in each group).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4522242&req=5

f2: Degradation of filensin. Western blot analysis with an anti-filensin antibody. A: The 94 kDa form of filensin is processed into the 50 kDa and 38 kDa forms in vivo (arrow). B: Western blot analysis with anti-β-actin antibody as an internal control. Lane 1: control group (G1). Lane 2: hesperetin-treated group (G2). Lane 3: selenite-treated group (G3). Lane 4: selenite and hesperetin-treated group (G4). M shows the molecular weight standards. C: The respective bar diagrams show the band intensity (densitometric value) of the 94 kDa (black bar), 50 kDa (gray bar), and 38 kDa (white bar) forms of filensin levels relative to the levels in the control G1 group. All bar diagrams are expressed as the mean ± SD, and statistical analysis was determined using the unpaired Student t-test. *p<0.05 versus control (G1 group) and †p<0.05 versus rats with selenite-induced cataracts without hesperetin treatment (G3 group; n = 9 in each group).
Mentions: The degradation of filensin in selenite-induced cataract lenses was investigated with western blot analysis. The lenses from rats in the G1 and G2 groups contained the same proportions of the 94 kDa, 50 kDa, and 38 kDa forms of filensin (Figure 2, lanes 1 and 2). The 94 kDa and 50 kDa forms of filensin were significantly less abundant in lenses from the G3 group than in lenses from the G1 and G2 groups (Figure 2, lane 3). However, the intensities of the 94 kDa and 50 kDa form of filensin in lenses were rescued with the hesperetin treatment with selenite administered to rats (Figure 2, lane 4). The protein expression of β-actin was detected as an internal control of all groups (Figure 2B). The 94, 50, and 38 kDa forms of filensin normalized for β-actin were assessed using densitometry, and data are depicted graphically in Figure 3C. The 94 kDa and 50 kDa forms of filensin were significantly decreased in the G3 group compared to the G1 and G2 groups, and hesperetin treatment for rat cataract (the G4 group) inhibited the protein loss observed in the selenite-induced rat cataracts (the G3 group). Administration of hesperetin and/or selenite did not affect the 38 kDa form of filensin.

Bottom Line: Lenses were observed with slit-lamp microscopy, and filensin degradation and the decreased glutathione (GSH) and ascorbic acid levels in the lens were measured on day 6.Expression of the 94 kDa and 50 kDa forms of filensin was significantly decreased in the lenses in the G3 group compared with those in the G1 and G2 groups.In the G3 group lenses, the GSH and ascorbic acid levels were lower than in the control group but were normalized in the G4 group lenses.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular Function and Physiology, Faculty of Pharmacy, Keio University ; Division of Hygienic Chemistry, Faculty of Pharmacy, Keio University.

ABSTRACT

Purpose: This study investigated the ability of hesperetin, a natural flavonoid, to prevent selenite-induced cataracts in a rat model.

Methods: Animals were divided into four treatment groups: G1 (control group), G2 (hesperetin-treated group), G3 (selenite-induced cataract group), and G4 (hesperetin-treated selenite cataract group). Animals in the G1 and G3 groups were injected with vehicle alone, while those in the G2 and G4 groups received a subcutaneous injection of hesperetin (0.4 μg/g bodyweight on days 0, 1, and 2, corresponding to P13, P14, and P15). Sodium selenite (20 μmol/g bodyweight given 4 h after the hesperetin injection on day 0) was administered to rats in the G3 and G4 groups to induce cataract formation. Lenses were observed with slit-lamp microscopy, and filensin degradation and the decreased glutathione (GSH) and ascorbic acid levels in the lens were measured on day 6.

Results: Lenses in the G3 group showed mature central opacity, while some lenses in the G4 group lacked central opacity and had lower-grade cataracts. All lenses in the G1 and G2 groups were transparent. Expression of the 94 kDa and 50 kDa forms of filensin was significantly decreased in the lenses in the G3 group compared with those in the G1 and G2 groups. Interestingly, these forms of filensin rescued the rat lenses in the G4 group. In the G3 group lenses, the GSH and ascorbic acid levels were lower than in the control group but were normalized in the G4 group lenses.

Conclusions: The results suggest that hesperetin can prevent selenite-induced cataract formation.

No MeSH data available.


Related in: MedlinePlus