TL;DR
FVP caused multifaceted oxidative, inflammatory, apoptotic, and hormonal damage in ovarian and uterine tissues, while BTN significantly reduced these effects, preserving tissue integrity and function.
This study aimed to investigate the effect of hesperidin (HSP) at two different doses on deltamethrin (DLM)-induced testicular damage. The study comprised four groups of Wistar Albino rats (n = 8 per group): Control, DLM, DLM + HSP 100 mg/kg, and DLM + HSP 300 mg/kg. At the end of the study, oxidative stress markers and CRP were measured in serum samples. Testicular tissues were assessed histopathologically. Expression of Bcl-2, Bax, and Nrf-2 were determined by immunofluorescence staining. RT-qPCR assessed tissue collagen (COL1A1, COL3A1) and apoptotic () expressions. HSP at both doses lowered the DLM-induced increase in total oxidant status, oxidative stress index (total oxidant status/total antioxidant capacity), and CRP levels. Nrf-2 was increased by a high dose of HSP (300 mg/kg). Whereas HSP normalized other apoptotic parameters at both doses, it partially normalized Bax expression in immunofluorescence and Bcl-2 expression in RT-qPCR only at 300 mg/kg. HSP reduced the increased fibrosis in DLM exposure, as revealed by the expressions of COL1A1 and COL3A1 at both doses. HSP partially ameliorated DLM-associated histological alterations, including Johnsen’s score, tubule diameter, and thickness of the tunica albuginea. HSP may exert protective effects against DLM-induced testicular injury by modulating systemic oxidative status, apoptosis-associated signaling, and profibrotic gene expression.
It has been observed that zingerone (ZNG), an antioxidant agent, may be a significant protective against APAP liver damage.
Doxorubicin (DOX) is an anticancer antibiotic that is widely utilized. Nevertheless, this therapeutic potential is hampered by its cardiotoxicity. Alogliptin (ALO), an antidiabetic, recently is being repurposed for the management of various organs ailments owing to its discovered biological activities as an antioxidant, anti-inflammatory, anti-apoptotic and antifibrotic through multiple pathways. This study is directed to evaluate the possible protective effect of ALO against DOX-induced cardiac molecular and histopathological alterations. Twenty-four adult Wistar rats were grouped into control in addition to ALO (20 mg/kg, p.o, 21 days), DOX (18 mg/kg, i.p; six equal divided doses on alternative days starting at day 8), and Dox + ALO treated groups. On the 21st day, blood samples are collected to assess cardiac biomarkers. Additionally, the hearts of all rats were separated and processed for histological evaluation, ultrastructural examination, and collagen content determination by Masson Triciumus staining, and biochemical studies. The DOX group had pronounced deleterious histological and ultrastructural disorganization accompanied with abundant collagen disposition. Biochemically, DOX group demonstrated significant elevation of cardiomyocytes content of MDA, NF-κB, TNF-α, IL-6, BAX, and TGF-β1 which mirrored as significantly elevated serum LDH, CKMB, and cTnI levels. However, SOD and CAT activities as well as GSH, BCL-2, SIRT3 and NRF2 content along with miRNA-133a gene expression are significantly decreased. Present results proved the prophylactic ALO antioxidant, anti-inflammatory, anti-apoptotic, and anti-fibrotic influence on the DOX-induced cardiotoxicity with proposed mechanisms entailing the activation of SIRT3 pathway that may be governed by miRNA-133a. However, these results are limited by the inspection lack of echocardiography or hemodynamic alterations, gain and loss of function, caspase activation, and mitochondrial health tests. Thus, ALO has the potential to be an appropriate therapy for DOX-induced cardiotoxicity.
FA-NIO targets oxidative stress-mediated apoptosis, attenuates NLRP3 inflammasome-related signaling, and restores steroidogenic function, thereby successfully attenuating DOX-induced testicular toxicity in rats.
Ischemia/reperfusion (IR) injury secondary to ovarian torsion results in oxidative stress, inflammation, and structural damage to the ovary. Silymarin (SLY), a natural flavonoid complex, possesses potent antioxidant and anti‐inflammatory effects. The present study was designed to evaluate the protective effects of SLY on ovarian IR injury. An experimental model of OIR was created, and animals were divided into Sham, OIR, and OIR + SLY groups. An acute single dose of silymarin (100 mg/kg) was given to the treatment group. Tissue and serum levels of TNF‐α, IL‐17, TGF‐β1, and H2O2 were determined, as well as TOS. Tissue oxidative stress parameters MDA, GSH content, and SOD activity were assessed. Histopathological evaluation of ovarian tissues was done. Compared to sham controls, the OIR group exhibited significantly higher tissue and serum inflammatory cytokine levels, and oxidative stress indicators, as well as higher MDA levels and lower GSH and SOD activity (p < 0.05). Histological analysis revealed significant vascular congestion, bleeding, and tissue deterioration. SLY therapy significantly decreased inflammatory cytokines and lipid peroxidation while increasing antioxidant defenses (p < 0.05). Histopathological results also showed improved ovarian tissue integrity in the treatment group. SLY may be used as an adjuvant treatment for ovarian torsion, as it reduces oxidative stress and inflammation in OIR injury of the ovary while preserving its histological structure.
The protective mechanism involves anti-oxidant enhancement and inhibition of oxidative stress-induced inflammation and apoptosis, supporting the therapeutic potential of HSP in managing phthalate-related renal injury.
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