This research aims to investigate the adverse effects of ZnO NP on ovarian tissue and the follicular and menstrual cycle and the protective effects of l-arginine on the aforementioned tissues. 30 rats were divided into five groups. The first group was the control group. The second and fourth groups received 100 mg/kg and 200 mg/kg ZnO NP, respectively. The third and fifth groups received the same doses of ZnO NP as the second and fourth groups, respectively. However, the third and fifth groups received an additional dose of 1.3 gr/kg of LA amino acid. ZnO NP and LA are given intraperitoneal for 21 days. Blood samples from each rat and a part of the ovarium were collected to test for gene expression and histological analysis. Compared to levels of housekeeping gene β-actine, levels of apoptosis effectors such as Bax, Bcl, Caspase 3, and Caspase 9 were significantly increased in all groups. In groups that received doses of LA (three and five), atretic follicle size was smaller compared to groups that did not receive LA (two and four). In addition, in the third group, the secondary and primordial follicle's generated oocytes were smaller compared with groups two, four, and five. Compared with the control group, all groups experienced morphological degeneration of follicles and tissue. ZnO NP has inevitable, morphological, and physiological effects on the ovary and can detrimentally impact the tissue. LA can aid in the regeneration of the tissue and block damage induced by stress and toxicity.

Objectives: Apigenin and parthenolide as natural products have potent antioxidant and anti-inflammatory outcomes that could make them a perfect option for endometriosis therapy. This study aimed to determine the effects of apigenin and parthenolide on created endometrial implants in a rat model of endometriosis. Methods: Thirty-nine mature, female Sprague-Dawley rats were assigned randomly to six experimental groups four weeks after endometriosis induction. Group 1 (n = 5): Control (CTRL) that opened and closed the abdomen; Group 2 (n = 6): Peritoneal and ovarian endometriosis (POE) + drug-free; Group 3 (n = 7): POE+ Apigenin (APG) (50 mg/kg); Group 4 (n = 7): POE+ Parthenolide (PTL) (10 mg/kg); Group 5 (n = 7): POE+ Apigenin (APG) (50 mg/kg) + Parthenolide (PTL) (10 mg/kg); Group 6 (n = 7): POE+ DMSO. An endometriosis model was created, and histopathological analysis and biochemical evaluation were performed. Serum and peritoneal levels of pro-and-anti-inflammatory cytokine, and oxidative stress of implant tissue were measured. Results: Serum IL-37 levels decreased significantly in the APG-treated group compared to the drug-free group (p = 0.016). The peritoneum and ovary endometriosis histopathologic scores were significantly lower in APG-treated (p = 0.001) and PTL-treated (p = 0.001) groups in comparison to the drug-free group. The oxidative stress index (OSI) values were increased statistically significantly in ovary endometriosis tissue in the drug-free group, (p = 0.001). However, compared to the drug-free group, OSI values decreased statistically significantly in the APG-treated group (p = 0.003).Conclusions: The application of apigenin caused a decrease in oxidative stress and an improvement in histopathological grade. Apigenin may be a novel therapeutic agent for the treatment of endometriosis.

Diabetes mellitus (DM) leads to renal damage through oxidative stress. Carvacrol (CAR), a monoterpenoid phenol, possesses anti-inflammatory and antioxidant properties. We investigated the potential effects of CAR on histological, gene expression, and biochemical parameters in a rat model of DM. Four groups were created: group 1, control; group 2 (n = 9), DM; group 3 (n = 9), DM + dimethyl sulfoxide (DMSO); and group 4 (n = 9), DM + CAR. DM was created by injecting streptozotocin (STZ). CAR (20 mg/kg) was prepared through dissolution in 0.1% DMSO. CAR and 0.1% DMSO were administered daily for 4 weeks to groups 4 and 3, respectively. At the end of this study, urea, creatinine, paraoxonase-1 (PON-1), and arylesterase (ARES) were measured in serum samples. Histopathological changes and expression of Nuclear factor erythroid 2–related factor 2 (Nrf-2) in renal tissues were assessed. Immunohistochemical(ihc) staining and RT-qPCR analysis were performed to evaluate apoptosis, focusing on Bax and Bcl-2gene expression. Masson’s trichrome(MT) staining and RT-qPCR analysis of COL1A1 and COL3A1 mRNA levels were used to assess fibrosis. Increased urea and creatinine levels in DM were significantly decreased after CAR administration. CAR application also improved reduced levels of PON 1 and ARES, which are associated with diabetes. Both immunohistochemistry and RT-qPCR analyses revealed that CAR therapy mitigated the diabetes-induced elevation in Bax and reduction in Bcl-2 expression. CAR treatment improved histopathological findings and renal Nrf-2 immunofluorescence(if) intensity. Furthermore, gene expression analysis demonstrated that COL1A1 and COL3A1 were upregulated in DM, while CAR administration downregulated them. In conclusion, CAR has a protective role in decreasing renal impairment linked to DM by regulating Bax and Bcl-2 levels and rectifying histological damage.

Objective: Cisplatin (CIS) is a frequently used chemotherapeutic drug; nevertheless, its clinical efficacy is limited by cardiotoxicity, mostly due to oxidative stress and apoptosis. Natural antioxidants such as S-Allyl-L-Cysteine (SAC) and Allyl Disulfide (ADS)—organosulfur compounds derived from garlic—exhibit potential in mitigating such damage. This study aimed to evaluate CIS-induced cardiotoxicity in rats and investigate the potential for SAC and ADS to reduce this toxicity. Methods: Four groups -Control, CIS, CIS + SAC, and CIS + ADS- were randomly assigned to thirty-two female Sprague Dawley rats. On days 1 and 8 of the experiment, CIS was given intraperitoneally at a dose of 5 mg/kg, and for 14 days in a row, SAC and ADS were given orally by gavage at a dose of 100 mg/kg. Using Hematoxylin-Eosin (H&E) and Periodic Acid-Schiff (PAS) staining, heart tissues were excised at the termination of the experiment and examined histopathologically. Results: In the CIS group, prominent histopathological changes, including interstitial congestion, lymphocytic infiltration, edema, and vacuolar degeneration in cardiomyocytes, were observed. PAS staining showed glycoprotein accumulation and chondromatous metaplasia. All these changes were reversed in either the CIS+SAC group or the CIS+ADS group by improving cardiac architecture and lowering levels of congestion, edema, and degeneration. Conclusion: This study shows that SAC and ADS have protective effects against CIS-induced cardiotoxicity. These natural antioxidants may be used to prevent cardiotoxicity that is induced by chemotherapy.