Saeed Alshahrani

The objective of the study was to evaluate the quality of Zamzam water, holy water for Muslims and consumed for its medicinal value. The present study demonstrates the physicochemical characterization and wound healing property of Zamzam water. The physicochemical characterization of Zamzam water samples was analyzed for dissolved oxygen, pH, conductivity, total dissolved solids, redox potential, zeta potential, polydispersity index, and zeta size. The microbial quality of Zamzam water was also assessed by exposing water samples to open air. In this work, Zamzam water was also screened for the medicinal value through wound healing properties in Wistar rats. Zamzam water exhibited a unique physicochemical characterization with high levels of dissolved oxygen, zeta potential, polydispersity index, redox potential, total dissolved solids, and conductivity before exposure to open air. After open air exposure, Zamzam water resisted the growth of bacteria. The wound healing properties of Zamzam water in vivo showed a 96% of healing effect on 12th day observation. The wound healing was achieved by modulating pro-inflammatory cytokine such as interleukin -1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor -α (TNF-α). Followed by the level of apoptosis markers caspase-9 and caspase-3 were reduced. The present study proved that Zamzam water is a good-quality water and showed excellent wound healing property. Therefore, Zamzam water can be used for pharmaceutical formulations.

The study investigated the wound healing effect of medicinal oil (MO) formulation prepared from Murraya koenigii leaves extract (methanolic) incorporated in olive oil. The MO was visually transparent, homogenous, smooth in texture, the viscosity grade was observed as 140 cP and easily spreadable. Pro-inflammatory cytokines IL-1β, IL-6, and TNF-α were significantly reduced to 82.3 ± 3.5, 156 ± 6.2, 137.3. ± 5.5 pg/ml, respectively after treatment with MO when compared to disease control animals that showed IL-1β, IL-6, and TNF-α levels of 170 ± 6, 265 ± 7, and 288.6 ± 11, pg/ml respectively. The level of pro-inflammatory cytokine in povidone iodine solution (PIS) group was 95.3 ± 3, 162 ± 6, 177.6 ± 8.9 pg/ml of IL-1β, IL-6, and TNF-α respectively. Interestingly, the wound-healing efficacy of MO was found better as compared to povidone iodine treated standard group and concluded that MO has excellent wound healing effect.

Background: Ursolic acid (UA) is a natural pentacyclic triterpenoid that is known for its benefits under several pathological conditions. Cisplatin (CP) is among the most preferred chemotherapeutic agents; however, its nephrotoxicity limits its clinical utility. Purpose: This study was aimed to determine the role of UA in the reduction of CP-induced nephrotoxicity and mitigation of pro-inflammatory cytokines and apoptosis in a rat model. Methodology: Male Wistar rats were randomized into vehicle control, CP (7.5 mg/kg), UA 10 mg/kg, and CP with UA 5 and 10 mg/kg groups. Kidney and blood samples were collected for assessment of renal function, measurement of pro-inflammatory cytokines, apoptosis markers, antioxidant activity, and tissue histology. Results: CP significantly increased the levels of serum Cr, BUN, and uric acid; it also induced histological damage reflecting the pathophysiology observed during nephrotoxicity. CP has also shown its pro-oxidant activity in kidney tissue because CP decreased the levels of GSH, SOD, and CAT; it increased the lipid peroxidation as measured by MDA content. In addition, CP significantly upregulated the activity of pro-inflammatory cytokines and expression of apoptotic markers, that is, there were increased levels of IL-1β, IL-6, TNF-α, caspase-3, and caspase-9. Two weeks of continuous treatment of UA showed significant recovery against CP-induced nephrotoxicity; UA decreased the levels of Cr, BUN, and uric acid and ameliorated histological damage. UA also downregulated the activities of IL-1β, IL-6, and TNF-α as well as expression of caspase-3 and caspase-9. Furthermore, CP-induced oxidative stress that was antagonized by UA—the levels of GSH, SOD, and CAT were significantly increased while MDA content was decreased. Conclusions: UA has a protective effect against CP-induced nephrotoxicity, which may be due to its antioxidant activity and mitigation of IL-1β, IL-6, TNF-α, and markers of apoptosis.