Objective: Cisplatin is an effective antineoplastic agent used in cancer therapy. However, the use of cisplatin is restricted due to its toxic side effects. Alleviation of its side effects which restricts cisplatin use is highly important. We aimed to investigate the effects of curcumin, vitamin E and their combination in cisplatin induced testicular apoptosis. Material and methods: Thirty-five Wistar albino male adult rats, weighing 300-350 g were divided randomly into five groups including seven rats in each as control, cisplatin, curcumin, vitamin E, and curcumin + vitamin E. On the posttest 5th day, rats were sacrificed, and their testes were removed. 4-5 µm sections from formalin fixed paraffin embedded testis tissues were stained both hematoxylin-eosin to analyze histologically and immunohistochemically to determine the expression of the apoptotic pathway proteins (Bax, Cas-3, Bcl-2). Results: Increased histological damage with cisplatin administration was reduced in treatment, especially in combination therapy. Cas-3 and Bax protein immunostaining intensities H-scores were significantly increased but Bcl-2 was slightly decreased in the cisplatin group compared to the control. In all treatment groups Bax, Cas-3 decreased compared to cisplatin group however Bcl-2 decreased in the curcumin and vitamin E groups. Bax/Bcl-2 was the highest in the cisplatin, and decreased in all treatment groups in favor of control. Conclusion: Cas-3 expression increased by cisplatin administration suggests that cisplatin causes apoptosis of germ cells. According to the present findings, cisplatin mainly caused testicular apoptosis through the Cas-3 and Bax apoptotic protein pathways. Cisplatin-induced testicular apoptosis can be prevented by administration of curcumin, vitamin E, and combination therapy. Cite this article as: Gevrek F, Erdemir F. Investigation of the effects of curcumin, Vit-E and their combination in cisplatin-induced testicular apoptosis using immunohistochemical technique. Turk J Urol 2018; 44(1): 16-23.

Diabetes mellitus and periodontitis are chronic inflammatory diseases that disrupt soft tissue metabolism. The diseases separately or together increase apoptosis in gingival fibroblast cells and reduce cell renewal. We investigated the effects of diabetes and periodontitis on the composition and structure of gingival connective tissue. We used gingival biopsies from 16 healthy individuals (control group, C), 16 type 2 diabetic patients with chronic periodontitis (diabetes + periodontitis group, D + P) and 16 healthy chronic periodontitis patients (periodontitis group, P). Biopsies were obtained under local anesthesia. Clinical attachment level (CAL), gingival index (GI) and plaque index (PI) were measured prior to gingival biopsies. Fibroblast cells were counted stereologically. Inflammatory cells were counted histomorphometrically. Hypoxia-inducible factor (HIF)-1α, lysyl hydroxylase (PLOD-2), neutrophil collagenase (MMP-8), and vascular endothelial growth factor (VEGF) levels were evaluated immunohistochemically. CAL, GI and PI for the C group were lower than for the other groups (p < 0.05). Fibroblast cell counts were lower for the D + P group than for the other groups (p < 0.05). Diabetes increased inflammatory cell numbers in the D and D + P groups compared to the C and P groups. MMP-8 levels were higher for the D + P group than for the other groups. VEGF was elevated in both the P and D + P groups compared to the C group, while HIF-1α and PLOD-2 levels were comparable. Diabetes increased tissue destruction and inflammation, and decreased fibroblast cell numbers without affecting collagen crosslinking and HIF-1α levels.