Objective: To investigate the effects of Borassus flabellifer L. extracts on antioxidant activity, maintenance of cellular redox, and mitochondrial function in cisplatin-induced kidney injury. Methods: The extracts of Borassus flabellifer were obtained from crude male flowers using ethyl acetate and methanol. The antioxidant potential was evaluated by 2,2-azino-bis-(3-ethylbenzothiazoline- 6-sulfonic acid), 2,2-diphenyl-1-picrylhydrazyl, and ferric reducing antioxidant power, and total phenolic content was also determined. Cytoprotective activity of ethyl acetate and methanolic extracts was assessed after kidney cells were treated with cisplatin. Oxidative stress was determined by glutathione (GSH) assay, and formation of reactive oxygen species (ROS) and changes in mitochondrial transmembrane potential (ΔΨm) using 2’,7’-dichlorofluorescin diacetate and JC-10 assays, respectively. Results: Borassus flabellifer methanolic extract exhibited greater antioxidant activity than the ethyl acetate extract. Cytoprotective effect was demonstrated in both extracts, particularly in the ethyl acetate extract. The extracts showed protection against the cytotoxic effect of cisplatin by prevention of the increased GSSG and declined GSH/GSSG ratio. Both extracts also prevented the increase in ROS formation, and loss of ΔΨm. Conclusions: Both Borassus flabellifer extracts show antioxidant activity and cytoprotective effect against cisplatin-induced cytotoxicity of NRK-52E cells by preventing oxidative stress and maintenance of GSH redox status. Borassus flabellifer extracts may possess beneficial effects on the prevention of oxidative stress- induced cell injury.

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Objective: To evaluate the effect of Heracleum persicum L. against gentamicin-induced nephrotoxicity in rats. Methods: Thirty-six Wistar rats were divided into 6 groups including control (normal saline), gentamicin (80 mg/kg/d for 10 d), Heracleum persicum (750 mg/kg/d), and gentamicin (10 d) + Heracleum persicum extract at three different doses (250, 500, and 750 mg/kg/d for 40 d). Urine creatinine, urea, protein, and albumin levels were determined. In addition, serum urea, creatinine, sodium, potassium, cytokines (TNF-α, IL-1β, IL-6, and IL-10), glutathione peroxidase activity, total antioxidant capacity, kidney malondialdehyde, stereological parameters, and expressions of apoptosis-related genes (p53, Bax, Bcl-2, and caspase-3) were measured. The LD₅₀ of Heracleum persicum extract was determined based on Lorke’s method. Histopathological evaluation was also performed. Results: In addition to decreased urine protein and albumin, and increased creatinine and urea, co-treatment with gentamicin and Heracleum persicum significantly reduced levels of creatinine and urea, and increased sodium and potassium in serum. Heracleum persicum treatment also improved stereological parameters and serum inflammatory cytokines. There was a significant increase in serum glutathione peroxidase activity and total antioxidant capacity as well as a reduction in malondialdehyde level. Furthermore, treatment with Heracleum persicum extracts downregulated p53, caspase-3, and Bax and upregulated Bcl-2 expressions. In histopathological evaluation, Heracleum persicum extracts showed protection against gentamicin-induced renal damages. Conclusions: Heracleum persicum exhibits protective effects against gentamicin-induced structural and functional renal impairments.

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Objective: To evaluate the anti-inflammatory potential of aqueous extract of Pterocarpus santalinus L.f. heartwood using molecular docking and in vivo experiment. Methods: An aqueous extract of Pterocarpus santalinus heartwood was prepared using a Soxhlet apparatus. Phytocompounds in the extract were tentatively identified using high-resolution mass spectrometry. Molecular docking experiments were carried out to evaluate the binding affinity of selected compounds, phloridzin to cyclooxygenase-1 (COX-1), cyclooxygenase-2 (COX-2), prostaglandin E synthase-1 (PGES-1) and 5-lipoxygenase (5-LOX). Anti-inflammatory potential was evaluated by carageenan induced paw edema model in rats. Results: The presence of major component phloridzin along with quercetin, parthenin, ginkgolide B, picrotoxinin, usnic acid, octopine, and epigallocatechin was detected in the extract. Molecular docking study showed that phloridzin inhibited COX-1, COX-2, PGES-1 and 5-LOX with more affinity than ibuprofen and paracetamol. Pterocarpus santalinus heartwood extract at 200 and 400 mg/kg BW showed significant reduction in carageenan-induced hind paw edema in a dose-dependent manner, but the effect was slow when compared with the standard ibuprofen (30 mg/kg p.o.). Conclusions: The study indicated that after clinical trials, the aqueous extract of Pterocarpus santalinus heartwood can be effectively used in phytotherapy to treat inflammation.

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Objective: To investigate the effect of Corchorus olitorius aqueous fraction (COAF) on quorum sensing (QS)-regulated virulence factors and biofilm formation in Pseudomonas aeruginosa (PAO1). Methods: The preliminary screening of the anti-QS effect of COAF was performed by evaluating the anti-pathogenic activity against Chromobacterium violaceum CV026 biosensor strain. Next, the inhibitory effects of COAF on QS-regulated pyocyanin production, proteolytic and elastolytic activities, swarming motility, and biofilm formation were evaluated in PAO1. Results: The results showed that the treatment of COAF significantly decreased the biofilm biomass, attenuated virulence factors, and inhibited swarming motility of PAO1 without affecting the growth of the bacteria in a dose-dependent manner. COAF at 2 000 μg/mL significantly decreased Las B elastase activity in PAO1 culture, exopolysaccharide production, swarming motility, pyocyanin level, and biomass of PAO1 by 55% (P<0.05), 60% (P<0.01), 61% (P<0.01), 65%(P<0.01) and 73% (P<0.01), respectively. In addition, the production of violacein was decreased by 62% (P<0.01) with the treatment of a high dose of COAF. Conclusions: These findings indicate that COAF can be a potential source of anti-QS agents.

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Objective: To investigate the anti-senescence effect of 3-bromo-4,5- dihydroxybenzaldehyde (BDB) from Polysiphonia morrowii Harvey in human dermal fibroblasts (HDF). Methods: HDF were subjected to treatment of BDB and then treated with hydrogen peroxide (H₂O₂) to induce premature senescence. Senescence-associated β-galactosidase (SA-β-gal) activity in HDF was determined using the SA-β-gal staining method. Intracellular reactive oxygen species (ROS) production was measured using the 2’,7’-dichlorodihydrofluorescein diacetate assay. Western blotting assay was performed to assess the level of antioxidant enzyme glutathione peroxidase 1 (GPX1). In addition, intracellular collagen and collagenase contents were analyzed using the respective ELISA kits. Elastase activity in HDF supernatants was measured from p-nitroaniline release and normalized using total protein content. Results: Treatment of HDF with H₂O₂ increased the activity of SAP-gal, but BDB pre-treatment resulted in the reduction of SA-β- gal activity. Moreover, BDB significantly reduced H₂O₂-induced intracellular ROS production. BDB also markedly increased the level of GPX1, which was inhibited by 400 µM of H₂O₂. Furthermore, in in vitro study, BDB significantly increased intracellular collagen content and decreased matrix metalloproteinase-1 and elastase activities in HDF. Conclusions: Our results demonstrate that BDB shows anti- senescence and anti-wrinkle activities in vitro.

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Objective: To investigate the potential anti-aging mechanism of 9-hydroxy-6,7-dimethoxydalbergiquinol (HDDQ) on hydrogen peroxide (H₂O₂)-induced oxidative stress in human dermal fibroblasts (HDFs). Methods: The effect of HDDQ on cell viability was assessed by MTT assay, and the effects of HDDQ on senescence-like phenotypes were determined by senescence-associated β-galactosidase (SA-β-gal) staining, Western blotting analysis, and a cell proliferation assay. The expression level and activity of sirtuin-1 (SIRT1) induced by HDDQ were also measured. Results: HDDQ reversed senescence-like phenotypes in the oxidant-challenged model, through reducing SA-β-gal activity and promoting cell growth. Meanwhile, decreases in ac-p53, p21^Cip1/WAF1, and p16^Ink4a and an increase in pRb were observed. HDDQ induced the expression of SIRT1 in a concentration- and time-dependent manner. Moreover, HDDQ inhibited H₂O₂-induced phosphorylation of Akt by SIRT1 up-regulation and reduced SA-β-gal staining. Conclusions: HDDQ inhibits H₂O₂-induced premature senescence and upregulation of SIRT1 expression plays a vital role in the inhibition of the senescence phenotype in HDFs.

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