Archives of oral biology · 2017
Hyperlipidemia is involved in apoptosis in rat submandibular glands.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
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Irie Koichiro, Tomofuji Takaaki, Ekuni Daisuke, Azuma Tetsuji, Yoneda Toshiki, Shimazaki Yoshihiro, Morita Manabu
Аннотация
OBJECTIVE: The aim of the present study was to investigate the effects of hyperlipidemia on histological changes and apoptosis in submandibular glands using apolipoprotein E (apoE)-deficient rats.
DESIGN: Histopathological findings related to induced apoptosis in the submandibular glands were compared between apoE-deficient rats (n=6; male; age, 16 weeks) and the corresponding wild-type rats (n=6).
RESULTS: ApoE-deficient rats showed significantly higher plasma levels of oxidized low-density lipoprotein (LDL), total cholesterol, very LDL and LDL, and lower plasma levels of high-density lipoprotein when compared to control rats (P<0.05). Lipid deposition in the submandibular gland was observed in apoE-deficient rat group and in none of the control group. Significant increases in vacuolization and apoptosis in acinar cells were observed in apoE-deficient rats, as compared to control rats (P<0.05). The number of active caspase-3-positive cells was also higher in the apoE-deficient rat group when compared with the control group (P<0.01).
CONCLUSIONS: According to our results, hyperlipidemia induced apoptosis in apoE-deficient rat submandibular glands. Oxidized LDL generation in case of hyperlipidemia may trigger off a reaction of apoptotic acinar cells with vacuolization in the submandibular glands.
DESIGN: Histopathological findings related to induced apoptosis in the submandibular glands were compared between apoE-deficient rats (n=6; male; age, 16 weeks) and the corresponding wild-type rats (n=6).
RESULTS: ApoE-deficient rats showed significantly higher plasma levels of oxidized low-density lipoprotein (LDL), total cholesterol, very LDL and LDL, and lower plasma levels of high-density lipoprotein when compared to control rats (P<0.05). Lipid deposition in the submandibular gland was observed in apoE-deficient rat group and in none of the control group. Significant increases in vacuolization and apoptosis in acinar cells were observed in apoE-deficient rats, as compared to control rats (P<0.05). The number of active caspase-3-positive cells was also higher in the apoE-deficient rat group when compared with the control group (P<0.01).
CONCLUSIONS: According to our results, hyperlipidemia induced apoptosis in apoE-deficient rat submandibular glands. Oxidized LDL generation in case of hyperlipidemia may trigger off a reaction of apoptotic acinar cells with vacuolization in the submandibular glands.