Effects of vitamin B12 on galectin-3, asprosin and pentraxin-3 levels in the kidney tissue of cisplatin applied rats

Introduction and Purpose: Cisplatin is an anticancer, antimicrobial and anti- inflammatory agent that is used effectively in the treatment of a wide variety of cancers and has serious side effects. The most common side effect that limits its use is nephrotoxicity. Various substances have been used as protective agents in drug- induced nephrotoxicities; One of these is vitamin B12. Pentraxin-3 (PTX3) is a member of the pentraxin family, which includes CRP, and is an inflammation-related glycoprotein that interacts with the complement system, and its levels are known to increase in both CKD and AKD. Galectin-3 (Gal-3) is an immunity-related carbohydrate-binding lectin and its expression increases in kidney damage. Asprosin is a hormone secreted mainly from white adipose tissue, but can also be secreted from different tissues and cells. It has been demonstrated that asprosin has an appetite-increasing effect during fasting and stimulates gluconeogenesis in the liver. Studies have shown that asprosin levels increase in diabetic kidney patients. The aim of our study is to investigate the protection of vitamin B12 in cisplatin-induced kidney damage and its effect on PTX3, Asprosin and Gal-3 expressions immunohistochemically in kidney tissue. Materials and Methods: In the experiment, 28 8-10 weeks old adult Wistar albino male rats were divided into 4 groups. No application was made to group 1 (group I, Control). A single dose of 5mg/kg cisplatin was administered intraperitoneally (i.p.) to group 2 at the beginning of the experiment (group II, Cisplatin). To group 3, a single dose of 5mg/kg cisplatin was administered at the beginning of the experiment, and then 4mg/kg vitamin-B12 was administered i.p. for 14 days (group III, Cisplatin+Vitamin B12). To group 4, 4 mg/kg vitamin-B12 was administered i.p. for 14 days (group IV, Vitamin B12). Kidney tissue samples were taken from rats in all groups and after washing with physiological saline, they were placed in 10% formaldehyde and stored under appropriate conditions for histological and immunohistochemical studies. After a week of post-fixation in 10% formol solution, routine tissue follow-up procedures were performed to perform light microscopic analyses. Sections of appropriate thickness were taken from the paraffin blocks prepared by routine histological monitoring with an automatic tissue tracking device. Afterwards, the sections were stained with the Hematoxylin-Eosin staining method and evaluated under a light microscope. Results: As a result of examining the sections under a light microscope; Kidney tissue was observed in its normal histological structure in the control and Vitamin B12 groups. Compared to the control group, significant atrophy of the glomeruli and a decrease in the Bowman space, degeneration of the proximal and distal tubule epithelium, and occasional hyaline cysts were observed in the Cisplatin group. Although there was a histopathologically significant decrease in the damage to the kidney tissue in the Cisplatin+Vitamin B12 group compared to the cisplatin group, the damage caused by cisplatin could not be completely eliminated. The immunoreactivity of asprosin was similar in the Control and Vitamin B12 groups (p = 0.446). Compared to the control, the immunoreactivity of asprosin increased statistically significantly in the Cisplatin group (p<0.001). Compared to the cisplatin group, asprosin immunoreactivity was observed to decrease statistically significantly in the Cisplatin+Vitamin B12 group (p<0.001). PTX3 immunoreactivity was similar in Control and Vitamin B12 groups (p=0.816). PTX3 immunoreactivity increased statistically significantly in the Cisplatin group compared to the control (p<0.001). Compared to the Cisplatin group, PTX3 immunoreactivity was observed to decrease statistically significantly in the Cisplatin+Vitamin B12 group (p<0.001). Gal-3 immunoreactivity was similar in the Control and Vitamin B12 groups (p=0.861). Gal-3 immunoreactivity increased statistically significantly in the Cisplatin group compared to the control (p<0.001). Compared to the Cisplatin group, Gal-3 immune reactivity was observed to decrease statistically significantly in the Cisplatin+Vitamin B12 group (p<0.001). Rats in all groups were sacrificed under anesthesia after blood was taken intracardiacally under anesthesia. Blood samples were centrifuged at 4000 rpm for 8 minutes and serum was taken. Serum samples were stored at -80°C until the date of analysis. In the biochemical study conducted to evaluate the serum total oxidant level (TOS) levels of all groups; TOS levels were similar in the Control and Vitamin B12 groups (p=0.209). Compared to the control group, TOS level increased statistically significantly in the Cisplatin group (p<0.001). Compared to the Cisplatin group, TOS levels decreased statistically significantly in the Cisplatin+Vitamin B12 group (p<0.001). In the biochemical study conducted to evaluate the serum total antioxidant level (TAS) levels of all groups; TAS levels were similar in the Control and Vitamin B12 groups (p=0.649). Compared to the control group, TAS level decreased statistically significantly in the Cisplatin group (p<0.001). Compared to the Cisplatin group, TAS levels increased statistically significantly in the Cisplatin+Vitamin B12 group (p<0.001). Conclusion: Vitamin B12 caused a decrease in PTX3, Gal-3 and asprosin immunoreactivities, which increased in cisplatin-induced nephrotoxicity, and findings indicating kidney damage. Vitamin B12 has a significant protective effect against cisplatin-induced kidney damage. Key words: Cisplatin, kidney damage, vitamin B12, PTX3, Asprosin, Gal-3