Rehab Fawzy Abdel-Rahman

Context: Alopecia affects a large population and current treatments have limited efficacy and tolerability. Essential oils have gained increasing interest as natural, low-risk alternatives. Aims: To evaluate the effects of Syzygium aromaticum and Rosmarinus officinalis oils, alone and in combination, on hair regrowth in rats and compared with 2% minoxidil. Methods: S. aromaticum oil was prepared by hydro-distillation, while R. officinalis oil was purchased from the local market and analysed by GCMS. Male Wistar rats (n=30) were randomized to negative control (vehicle), 2% minoxidil, S. aromaticum oil, R. officinalis oil, and a S. aromaticum-R. officinalis oil mixture groups. Treatments were applied topically on a shaved dorsal skin area once a day for 35 days. The times required for hair growth initiation and completion were recorded, along with hair growth scores on days 7, 21, and 35. On day 35, hair weight, length, and thickness were measured, and skin histology was examined. Results: All active treatments showed significant improvements in hair regrowth parameters manifested by a significant reduction in the duration of hair initiation and completion and improvement in all the measured parameters. The effects of S. aromaticum oil and R. officinalis oil on hair re-growth were comparable to that of minoxidil. The oils mixture demonstrated superior performance to minoxidil in terms of faster regrowth initiation (6.5 days), completion (21.83 days), and higher hair weight (22.2 mg/cm²) and length (16.67 mm). Histology indicated a higher follicle density in treated groups. Conclusions: The oils mixture exhibited an additive effect, outperforming minoxidil in promoting hair regrowth.

HIGHLIGHTS Induction of obesity in rats was done using a high-fat diet (HFD) and tap water containing 25% sucrose for a duration of 16 weeks. Obese control group exhibited significant increases in body weight, body mass index, waist circumference, dyslipidemia. Increase in cardiac injury markers, oxidative stress, altered adipokine levels, and impaired liver and kidney function in obese group were detected. Obese control group exhibited elevated levels of leptin and reduced levels of adiponectin, reflecting an imbalance in adipokine signaling. Apigenin modulated various signaling pathways involved in lipid metabolism, glucose homeostasis, and adipogenesis, as well as exert protective effects against oxidative stress.

A novel class of antidiabetic drugs known as sodium-glucose cotransporter 2 inhibitors (SGLT2-Is) prevents the renal proximal tubules from reabsorbing glucose. While a recent study showed that SGLT2-Is may be able to slow the proliferation of cancer cells that express SGLT2, limited evidence exists regarding their effects on renal cell carcinoma (RCC). Here, we examine the ability of the SGLT2-I canagliflozin (Cana) to prevent experimentally induced kidney carcinogenesis in male rats. A total of twenty-four rats were divided into four groups, six in each: negative control, DEN/TAA control; rats (60–70 g) were fed a choline-deficient diet (CDD) for 4 weeks, then rats were subjected to four doses of 50 mg/kg diethyl nitrosamine (DEN) over 8 weeks followed by thioacetamide 100 mg/kg (TAA) intraperitoneal injections twice weekly for 15 weeks, treated groups: rats were given canagliflozin (10 and 20 mg/kg b.wt.) orally starting from the 24th week of the experiment till the end of the 29th week. The obtained findings showed that treatment with canagliflozin reduced renal oxidative stress and toxicity indicator levels and considerably reinforced renal antioxidant capacity. The histological changes further supported the biochemical findings. In addition, canagliflozin therapy activated AMPK and inhibited Nrf2, NLRP3 and IL-6/STAT3 pro-inflammatory pathway. Immunohistochemistry exhibited upregulation of pro-apoptotic protein caspase-3 and downregulation of PCNA expression in Cana-treated groups. Conclusion: the results showed that canagliflozin has anti-carcinogenic efficacy against renal carcinogenesis via activating AMPK and suppressing NLRP3/IL-6/STAT3 signaling pathways.

Ferula assa-foetida known as Asafoetida has a long-established history in folk medicine as a therapeutically useful drug in many disorders. The current paper explored the in vivo and in vitro anti-inflammatory activities of the plant. Liquid ethanol crude extract was subjected to liquid-to-liquid extraction, and the fractions so obtained were evaluated against the carrageenan-induced acute paw edema model in rats, to determine the anti-inflammatory effects. The fractions that gave the greatest activity-ethyl acetate and hexane- afforded four sesquiterpene coumarins: auraptene ( 1 ), umbelliprenin ( 2 ), galbanic acid ( 3 ), and kamolonol ( 4 ). The overall structure was determined through detailed spectroscopic investigation, ¹ H NMR, ¹³ C NMR, DPET135, COSY, HSQC, HMBC, HRESIMS, and other references to the literature. Evaluation of the in vitro activity of the LPS stimulated RAW 264.7 macrophages showed that the compound 4 (ethyl acetate fraction) exhibited maximum inhibitory action against the generation of nitric oxide (NO), followed by the compounds 1 and 2 of the hexane fraction. Internet Pharmacology, Molecular Docking and Molecular dynamic simulation analysis were used to identify the target genes and explain the potential differences between the active compounds. As far as the authors know, there are no earlier reports that mention the anti-inflammatory action of kamolonol ( 4 ).

Hepatocellular carcinoma (HCC) is the most prevalent type of primary liver cancer. Many medications that had been used for a long period to treat the illness were eventually stopped due to negative effects or the development of drug resistance in HCC patients. Canagliflozin (CANA), a sodium-glucose cotransporter 2 (SGLT2) inhibitor, showed in vitro anti-carcinogenic efficacy against various cancer models’ other livers. The current study used rat models to examine canagliflozin’s therapeutic role against experimentally induced HCC. A total of 32 rats were divided into four groups, eight in each: negative control; HCC control: rats were fed a choline-deficient diet (CDD) and subjected to diethyl nitrosamine and thioacetamide (DEN/TAA) injections for 15 weeks; and treated groups: rats were given CANA (10 and 20 mg/kg b.wt.) orally from the 7th week of the experiment till the end. All the measured markers of HCC, liver function, and inflammatory markers were elevated in the HCC control group compared to the negative control (CTRL). Regarding immunohistochemistry, the HCC group showed downregulation in caspase-3 expression and upregulation in PCNA expression. On the other hand, canagliflozin-treated groups showed dose-dependent improvement in the measured parameters associated with HCC. Moreover, canagliflozin therapy ameliorates the histopathological alterations in HCC-induced rats. Taken together, CANA exhibits anti-HCC effects by activating AMP-activated protein kinase (AMPK) and suppressing the HIF-1α/YAP/TAZ pathway, making it a forthcoming therapeutic option for HCC.

Ischemia-reperfusion (IR) injury is a major cause of multiple organ failure. The purpose of this study was to look into the role of Tephrosia purpurea (TEP) and its active constituent pseudosemiglabrin (PS) in alleviating severe acute pancreatitis and its associated acute lung injury. We established a rat pancreatic IR model, and the rats were treated with TEP (200 mg/kg and 400 mg/kg) and PS (20 and 40 mg/kg), in addition to the IR control and sham groups. The results showed that the respiratory parameters, including inspiratory time (Ti), expiratory time (Te), duration (Dr), and respiratory rate (RR), were comparable among all groups, while peak inspiratory flow (PIF), forced vital capacity (FVC), and forced expiratory volume at 0.1 s (FEV₀.₁) were significantly impaired. Notably, PS at 40 mg/kg showed normal PIF, FVC, and FEV₀.₁/FVC compared to the IR group, indicating an improved lung function. Additionally, TEP and PS showed protective effects on pancreatic and lung tissues compared to the IR control group, with the following effects: alleviating pathological damage; reducing serum levels of trypsinogen activation peptide (TAP), lipase, and amylase; decreasing oxidative stress markers such as MDA and MPO; restoring antioxidant enzyme activity (GPx); suppressing inflammatory markers TNF-α, IL-6, and NF-κB; downregulating HMGB1 gene in pancreatic tissue; and upregulating the IL-22 gene in lung tissues. In conclusion, the obtained findings demonstrate that oral supplementation of TEP and PS to rats with pancreatic IR alleviates pancreatic and lung injuries by reducing oxidative stress and modulating inflammatory processes, which offers an attractive therapeutic option for severe acute pancreatitis and its associated acute lung injury.

Ischemia-reperfusion (IR) injury is a major cause of multiple organ failure. The purpose of this study was to look into the role of Tephrosia purpurea (TEP) and its active constituent pseudosemiglabrin (PS) in allevi-ating severe acute pancreatitis and its associated acute lung injury. We established a rat pancreatic IR model. Rats were treated with TEP (200 mg/kg and 400 mg/kg), and PS (20 and 40 mg/kg). In addition to IR-control and sham groups. The results showed that the respiratory parameters including inspiratory time (Ti), expiratory time (Te), duration (Dr), and respiratory rate (RR) were comparable among all groups while peak inspiratory flow (PIF), forced vital capacity (FVC), and forced expiratory volume at 0.1 sec-onds (FEV0.1) were significantly impaired. Notably, PS at 40 mg/kg showed normal PIF, FVC and FEV0.1/FVC compared to IR group indicating an improved lung function. Additionally, TEP and PS showed protective effects on pancreatic and lung tissues by alleviating the pathological damage, reducing serum levels of trypsinogen activation peptide (TAP), lipase, and amylase, decreasing oxidative stress markers MDA, GPx, and MPO, suppressing inflammatory markers TNF-α, IL-6, and NF-κB, downregulating HMGB1 gene in pancreatic tissue, and upregulating IL-22 and Th22 genes in lung tissues compared with the IR control group. In conclusions, the obtained findings demonstrate that oral supplementation of TEP and PS to rats with pancreatic IR alleviates pancreatic and lung injuries by reducing oxidative stress and modulation of inflammatory processes, which offers an attractive therapeutic option for severe acute pancreatitis and its associated acute lung injury.

Oleuropein (OLP) is a naturally occurring phenolic compound in olive plant with antioxidant and anti-inflammatory potential and can possibly be used in treating pancreatic injuries. This investigation aimed to follow the molecular mechanism behind the potential therapeutic effect of OLP against pancreatic injury persuaded by ischemia–reperfusion (I/R). Pancreatic I/R injury was induced by splenic artery occlusion for 60 min followed by reperfusion. Oral administration of OLP (10 and 20 mg/kg) for 2 days significantly alleviated I/R-persuaded oxidative damage and inflammatory responses in pancreatic tissue as indicated by the decreased malondialdehyde (MDA) content and increased glutathione peroxidase (GPx) activity, accompanied by the suppression of myeloperoxidase (MPO) activity and reduced levels of interleukin-1beta (IL-1β), nuclear factor kappa B (NF-κB), and tumor necrosis factor alpha (TNF-α) in pancreatic tissues. Furthermore, OLP treatment markedly restored the serum levels of amylase, trypsinogen-activated peptide (TAP), and lipase, with concurrent improvement in pancreatic histopathological alterations. Moreover, treatment with OLP regulated the pancreatic expression of inducible nitric oxide synthase (iNOS) and high-mobility group box 1 (HMGB1) relative to rats of the pancreatic IR group. Thus, OLP treatment significantly alleviates the I/R-induced pancreatic injury by inhibiting oxidative stress and inflammation in rats through downregulation of HMGB1 and its downstream NF-κB signaling pathway.