Search

GA3 is widely used as a growth stimulant in agricultural regions. The long‐term use of GA3 can cause organs damage. Chrysin is a flavonoid found in nature that is commonly used to treat organ toxicity. In this study, we examined the effect of chrysin on the testes function of GA3‐affected rats. A total of 24 male Wistar rats were divided into 4 groups. Saline was given to the control group. The chrysin group was given orally 50 mg/kg/BW of chrysin in saline. The GA3 group received a daily oral gavage of GA3 (55 mg/kg/BW). The protective group (chrysin + GA3) was given chrysin and GA3 as those described in chrysin and GA3 groups. There were an increase in MDA levels in the serum and testicular tissue of GA3‐treated group. Catalase, GSH, and SOD levels were all lowered in the GA3‐treated rats. Chrysin dramatically reduced the harmful effects of GA3 by restoring reproductive hormone levels, altered sperm parameters, and antioxidant capabilities. Furthermore, GA3 reduced the quantitative expression of steroidogenesis genes StAR and 3‐HSD, as well as Bcl2 genes, while it increased the apoptotic marker BAX; all were alleviated by the pre‐administration of chrysin. The pre‐administration of chrysin protected the GA3 group from spermatogenic vacuolation, interstitial edema, necrosis, and depletion. Chrysin inhibited oxidative stress and modulated antioxidant activity, as well as apoptosis‐/anti‐apoptosis‐related mediators in the testes. Chrysin has the potential to repair GA3‐induced testicular dysfunctions. This suggests that chrysin is preferable as a medication to mitigate GA3‐induced oxidative damage in the testes. Practical applications: Chrysin has the potential to repair GA3‐induced testicular dysfunctions. This suggests that chrysin is preferable as a medication to mitigate GA3‐induced oxidative damage in the testes. [ABSTRACT FROM AUTHOR]

Thyme (Thymus vulgaris) is an herbal plant with pleiotropic medicinal properties. In this study, we examined the possible protective effect of an ethanolic extract of thyme leaves against the renal oxidative stress induced by sodium nitrite (NaNO2). Male Swiss mice received either saline or thyme extract for 15 days (0.5 g/kg body weight, orally). NaNO2 (60 mg/kg) was injected intraperitoneally at Day 14. The protective group received the thyme extract for 15 days and NaNO2 on Day 14. Blood and kidney samples were taken from all groups to measure serum urea, blood urea nitrogen (BUN), creatinine, serum, tissue antioxidant activity, and the inflammatory cytokines IL‐1β and IL‐6. Quantitative real‐time PCR (qRT‐PCR) was used to examine the expression of kidney injury marker‐1 (Kim‐1), TNF‐α, nuclear factor erythroid‐2 related factor 2 (Nrf2), and hemoxygenase‐1 (HO‐1), all of which are associated with kidney redox and oxidative stress. Pretreatment with thyme extract reduced the effects of NaNO2 on urea, BUN, and creatinine, and reversed its effect on tissue and serum antioxidants. NaNO2‐induced nephritis as demonstrated by the upregulation in mRNA expression of Kim‐1 and TNF‐α, which was, however, recovered and protected by pretreatment with thyme extract. Expression of Nrf2 and HO‐1 was upregulated by treatment with thyme extract and downregulated by NaNO2 intoxication. NaNO2‐induced congestion in glomeruli and dilatation of the renal tubules, conditions that were restored in the group pretreated with thyme extract. NaNO2 upregulated Bax immunoreactivity and caused apoptosis in renal structures. Thus, thyme extract is effective in managing the renal toxicity associated with oxidative stress and renal redox. Practical applications: The results from this study have shown that use of thyme extract may promote better health due to its high antioxidant activity. For instance, it could be ingested to alleviate the symptoms of renal inflammation and oxidative stress associated with nitrite toxicity. Thyme extract regulated renal redox, oxidative stress, antioxidant levels, and inflammation‐associated genes at the molecular, biochemical, and cellular immunohistochemical levels. [ABSTRACT FROM AUTHOR]

The extensive usage of gibberellic acid (GA3) in agriculture and plant growth is generally associated with enormous human and public health hazards. The present research assesses the impact of n-acetyl cysteine (NAC) on the hepatorenal injury persuaded by GA3 for this purpose, After two weeks of adaptation twenty-four rats allocated into four groups (6 rats/group) as follows: control group, supplied with saline only; n-acetyl cysteine (NAC) group, provided with 150 mg/kg/bw by stomach tube (orally) dissolved in saline; Positive GA3 group, received GA3 (55 mg/kg/bw) orally; Protective group received NAC (150 mg/kg/bw) and GA3 (55 mg/kg/bw) as in NAC and GA3 groups. Rats received their treatments for consecutive 3 weeks. On day 22, rats were anesthetized, then euthanized. Blood and tissue samples were obtained for biochemical, antioxidants markers analysis, gene expression, and histopathological examination. Our results revealed significant changes in serum AST, ALT, urea, uric acid, total protein, and albumin levels with a substantial rise of MDA and NO concentration in GA3 treated rats along with a considerable decrease of the GSH and overexpression of the inflammatory hepatic and renal cytokines (IL-10, TNF-α, NOS) and fibrotic gene expression TGF-β1, and α-SMA, with boost expression of nuclear factor-kappa (NFkB). NAC co-administered with GA3 significantly normalized the kidney and liver function and the antioxidant state, besides normal histological structure of both liver and kidney tissue and downregulated expression of the pro-inflammatory cytokines as well as, fibrogenic gene expression. Practical applications: The current study confirmed that GA3 induced hepto-renal dysfunction that was ameliorated by NAC administration. Moreover, our findings confirmed the antioxidant capability of n-acetyl cysteine and afford robust evidence about the ameliorative effect of the n-acetyl cysteine to attenuate the hepatorenal injury induced by gibberellic acid through modulation of the antioxidant defense system fibrogenic, and pro-inflammatory cytokines expression. [ABSTRACT FROM AUTHOR]

Abnormal uric acid level result in the development of hyperuricemia and hallmark of various diseases, including renal injury, gout, cardiovascular disorders, and non‐alcoholic fatty liver. This study was designed to explore the anti‐inflammatory potential of stevia residue extract (STR) against hyperuricemia‐associated renal injury in mice. The results revealed that STR at dosages of 150 and 300 mg/kg bw and allopurinol markedly modulated serum uric acid, blood urea nitrogen, and creatinine in hyperuricemic mice. Serum and renal cytokine levels (IL‐18, IL‐6, IL‐1Β, and TNF‐α) were also restored by STR treatments. Furthermore, mRNA and immunohistochemistry (IHC) analysis revealed that STR ameliorates UA (uric acid)‐associated renal inflammation, fibrosis, and EMT (epithelial‐mesenchymal transition) via MMPS (matrix metalloproteinases), inhibiting NF‐κB/NLRP3 activation by the AMPK/SIRT1 pathway and modulating the JAK2‐STAT3 and Nrf2 signaling pathways. In summary, the present study provided experimental evidence that STR is an ideal candidate for the treatment of hyperuricemia‐mediated renal inflammation. Practical applications: The higher uric acid results in hyperuricemia and gout. The available options for the treatment of hyperuricemia and gout are the use of allopurinol, and colchicine drugs, etc. These drugs possess several undesirable side effect. The polyphenolic compounds are abundantly present in plants, for example, stevia residue extract (STR) exert a positive effect on human health. From this study results, we can recommend that polyphenolic compounds enrich STR could be applied to develop treatment options for the treatment of hyperuricemia and gout. [ABSTRACT FROM AUTHOR]

This work aimed to identify novel angiotensin‐converting‐enzyme (ACE) inhibitory peptides from Macadamia integrifolia antimicrobial protein 2 (MiAMP2). The MiAMP2 protein was hydrolyzed through in silico digestion, and the generated peptides were screened for ACE inhibitory activity. The in silico enzyme digestion results revealed that 18 unreported peptides were obtained using AHTPDB and BIOPEP‐UWM, and none were thought to be toxic based on absorption, distribution, metabolism, and excretion (ADMET) prediction. PGPR, RPLY, MNPQR, and AAPR were predicted to exhibit good biological activity. The molecular docking results revealed that the four peptides tightly bound to the active pocket of ACE via hydrogen bonds and hydrophobic interactions, among which RPLY and MNPQR bound to ACE more strongly. The in vitro assay results confirmed that RPLY and MNPQR peptides inhibited ACE via competitive manner. These results provide theoretical guidance for the development of novel foodborne antihypertensive peptides from Macadamia nut proteins. Practical applications: This study provides new insight on the inhibitory potential of Macadamia nut peptides against ACE, which may be further applied to the development of antihypertensive peptides in the medical industry. [ABSTRACT FROM AUTHOR]