Hyperlipidemia is involved in apoptosis in rat submandibular glands

Publication date: September 2017
Source:Archives of Oral Biology, Volume 81
Author(s): Koichiro Irie, Takaaki Tomofuji, Daisuke Ekuni, Tetsuji Azuma, Toshiki Yoneda, Yoshihiro Shimazaki, Manabu Morita
ObjectiveThe 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.DesignHistopathological 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).ResultsApoE-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).ConclusionsAccording 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.



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