Hormonal and inflammatory modulatory effects of hesperidin in hyperthyroidism-modeled rats

Abstract

The goal of the current study was to investigate the hormonal modulatory efficiency of hesperidin, through its regulatory potential of immunological, inflammatory, and/or antioxidant changes in on hyperthyroidism modeled adult female albino rats. Both normal and hyperthyroidism modeled rats (140-160g) were randomly divided into four groups (10 animals each) as follows: 1) healthy animals were daily ingested with saline for six weeks, and served as control group, 2) healthy animals were intraperitoneally injected with hesperidin (50 mg/kg/day) for a similar period, 3) hyperthyroidism-modeled animals without any treatment acted as positive control, and 4) hyperthyroidism-modeled animals were treated intraperitoneally with hesperidin for a similar period. The findings showed that hesperidin significantly modulated hyperthyroidism deteriorations, this was evidenced by a remarkable decline in serum T4, FT4, T3, FT3, TNF-α, IL1β-, IL4-, IL-6, and IL-10 levels, with a minor increase in TSH and significant raise in CD4+ level. Similarly, valuable improvement was observed in the oxidative status; serum SOD, GPx, CAT, and GSH levels were dramatically enhanced, associated with remarkable drop in MDA and NO levels. Also, hesperidin demonstrated nephro-hepatoprotective and anti-atherogenic potential, this was achieved from the notable reduction in ALAT and ASAT activities as well as urea, creatinine, cholesterol, and triglyceride close to the corresponding values of healthy group. These findings were supported by histological and immunohistochemical ones that showed a notable decrease in the expression of the calcitonin antibody. In conclusion, hesperidin possesses anti-hyperthyroidism, immunoinflammatory regulatory, and antioxidant activities that evidenced from the improvement of physio-architecture of the thyroid gland, reduction of inflammation and restoration of the impaired oxidative stress. This effect might be mechanized through immunological, inflammatory, apoptotic, and/or antioxidant modulatory pathways.

Melissa officinalis extract palliates redox imbalance and inflammation associated with hyperthyroidism-induced liver damage by regulating Nrf-2/ Keap-1 gene expression in γ-irradiated rats

“…The obtained data exhibited a notable elevation in the levels of the oxidative stress markers MDA and NO with marked depletion of both non-enzymatic (GSH) and enzymatic (SOD, CAT, and GPx) antioxidants in the hepatic tissues of the hyperthyroid rats due to the prolonged ROS production as well as consumption of the antioxidant defence system components. These results are in line with previous results of Panda et al [ 29 ] and Ashry et al [ 52 ]. Additionally, Kochman et al [ 53 ] reported that the oxidative damage of cellular membrane lipids in hyperthyroid was higher than in euthyroid individuals.…”

“…Lyu et al [ 65 ] revealed overexpression of hepatic pro-inflammatory genes (IL-6 and TNF-α) due to hepatic deficiency of Nrf2. Owing to this, the excessive production of pro-inflammatory cytokines in the hepatic tissues of the hyperthyroid rats is assured by the upregulated mRNA expression of both TNF-α and MCP1 which is consistent with the results of Bahtiyar et al [ 44 ] and Ashry et al [ 52 ]. Queck et al [ 66 ] reported that activation of the hepatic macrophage during liver injury was associated with upregulation of the hepatic MCP-1 which in turn activates fibrogenic hepatic stellate cells (HSCs) [ 67 ].…”