Effect of Quercetin on Cadmium-Induced PERK-CHOP Apoptosis Pathway in Rat Testis
Effect of Quercetin on Cadmium-Induced PERK-CHOP Apoptosis Pathway in Rat Testis
Bingzhao Yan1, Guiping Chen2, Lulu Ding1, Ruxue Huang1, Wenjing Yu1 and Jicang Wang1*
ABSTRACT
Cadmium is a heavy metal that is toxic and poisonous to the human body and could cause damage to different organs of the body, including testicles. Quercetin (Que), which is widely distributed in fruits and plants, belongs to the class of flavonoids and is thought to have health benefits and protect many tissues from heavy metals. This experiment aimed to explore the effect of Que on Cd-induced PERK-CHOP apoptosis pathway in rat testis. A total of 24 8-week-old Sprague–Dawley rats were divided into four groups: control group, CdCl2 group, CdCl2+Que group, and Que group. The control group was gavaged daily with distilled water and 0.9% sodium chloride solution, and the Cd and/or Que-treated groups were treated by daily intraperitoneal injection of CdCl2 solution and/or daily Que solution by gavage, respectively. Body weight, testis organ coefficient, and morphological changes of testis were measured. The related genes and protein expression levels of the PERK-CHOP pathway were also detected. The results showed that body weight and testicular organ coefficient decreased in cadmium-exposed rats compared with the control group, and pathological tissue sections showed atrophy of the internal convoluted vasculature structure, pathological conditions such as testicular interstitial cell hyperplasia, nuclear consolidation, and cell necrosis in cadmium-stained rats, and an increase in the number of apoptotic cells in the testis of TUNEL. In addition, cadmium exposure significantly increased the mRNA and protein expression levels of PERK, CHOP, ATF4, eIF2α, GRP78, and the pro-apoptotic factor Bax, while the expression of the apoptosis inhibiting factor Bcl-2 was significantly decreased, and compared with the CdCl2 group, the CdCl2 + Que group showed significantly decreased gene expression of PERK, CHOP, ATF4, eIF2α, GRP78, and Bax and Bcl-2 gene expression increased significantly, indicating that Que significantly attenuated Cd induced testicular toxicity. In conclusion, Que attenuates Cd toxicity and reduces apoptosis in rat testis by inhibiting the expression of mRNA and proteins involved in the PERK-CHOP pathway.
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