The primary objective of this study was to ascertain the anti-biofilm and anti-virulence properties of sub-minimum inhibitory concentration (MIC) levels of eugenol against the standard strain PAO1 and two multi-drug resistant P. aeruginosa clinical isolates utilizing quorum sensing inhibition (QSI). Eugenol at 400 μM significantly reduced biofilm formation on urinary catheters and the virulence factors (VF) including extracellular polysaccharides, rhamnolipid, elastase, protease, pyocyanin, and pyoverdine (p < 0.001). Further, eugenol exhibited a marked effect on the production of QS signals (AIs) (p < 0.001) without affecting their chemical integrity. In silico docking studies demonstrated a stable molecular binding between eugenol and QS receptor(s) in comparison with respective AIs. Investigation on reporter strains confirmed the competitive binding of eugenol to a QS receptor (LasR) as the possible QSI mechanism leading to significant repression of QS associated genes besides the VF genes (p < 0.001). This study provides insights, for the first time, into the mechanism of the anti-virulence properties of eugenol.

The symptoms of acute kidney injury (AKI) include a sudden drop-in glomerular filtration rate (GFR), a rise in serum creatinine (sCr), blood urea nitrogen (BUN), and electrolytes, which leads to a rapid loss of kidney function. Chronic kidney disease progresses when AKI symptoms persist for over three months or 90 days. Numerous prevalent secondary risk factors, including diabetes, hypertension, obesity, and heart illness, are directly or indirectly linked to the development of AKI and the switch from AKI to CKD. Recently, the change of intestinal bacteria known as "gut dysbiosis" has been linked to distant organ dysfunction, including the heart, lungs, kidneys, and brain. Indirectly or directly, gut dysbiosis contributes to the progression of CKD and AKI. However, the effects of gut dysbiosis and the mechanism of action in the progression from AKI to CKD are unknown or need further investigation. The mechanism by which gut dysbiosis initiates AKI's progression to CKD should be explicitly concerned. The review primarily focuses on the action of gut dysbiosis in kidney disease, the effects of dysbiosis, the characterisation of dysbiosis and its pathogenic products, the various pathogenic routes and mechanism involved in expediting the transition from AKI to CKD. We identified and briefly reviewed the impacts of dysbiosis in various situations such as hypoxia, mitochondrial induced reactive oxygen species (mtROS), aryl hydrocarbon receptor (AhR) activation and microbiota derived uremic toxemic substances profoundly to push AKI to CKD conditions.

Objective: Aged garlic extract (AGE) has been proven to exhibit antioxidant, hypolipidemic, hypoglycemic and antidiabetic properties. However, its effect on diabetic nephropathy was unexplored. Therefore, the present study was designed to investigate the renoprotective effect of AGE in streptozotocin-induced diabetic rats. Materials and Methods: Albino Wistar rats were induced with diabetes by a single intraperitoneal injection of 45 mg/kg b.w. of streptozotocin. Commercially available AGE was supplemented orally at a dose of 500 mg/kg body weight/day. Aminoguanidine, which has been proven to be an anti-glycation agent was used as positive control and was supplemented at a dose of 1 g/L in drinking water. The serum and urinary biochemical parameters were analyzed in all the groups and at the end of 12 weeks follow up, the renal histological examination were performed using H & E and PAS staining. Results: The diabetic rats showed a significant change in the urine (P < 0.001) and serum (P < 0.01) constituents such as albumin, creatinine, urea nitrogen and glycated hemoglobin. In addition, the serum lipid profile of the diabetic rats were altered significantly (P < 0.05) compared to that of the control rats. However, the diabetic rats supplemented with aged garlic extract restored all these biochemical changes. The efficacy of the extract was substantiated by the histopathological changes in the kidney. Conclusion: From our results, we conclude that aged garlic extract has the ability to ameliorate kidney damage in diabetic rats and the renoprotective effect of AGE may be attributed to its anti-glycation and hypolipidemic activities.