Free Radicals and Antioxidants

Rodent Models of Streptozotocin-Induced Diabetes as Suitable Paradigms for Studying Diabetic Kidney Disease

Haoxin Liu, Yucheng Wang, Ying Wang, Liang-Jun Yan — Sun, 01 Sep 2024 00:00:00 +0000

The purpose of this correspondence is to highlight the usefulness of Streptozotocin (STZ)-induced type 1 diabetes for studying Diabetic Kidney Disease (DKD) which is also known as diabetic nephropathy.1 DKD is a major microvascular complication of diabetes regardless of type 1 or type 2 diabetes. DKD is also a leading cause for the development of end stage renal failure.1 The main features of DKD is thickening of the glomerular basement membrane caused by accumulation of matric glycoproteins and collagens, resulting in increased albumin secretion and a decreased glomerular filtration rate. Read more. . .

In vitro and in silico Acetylcholinesterase Inhibitory Activity of Premna serratifolia Linn.

Sun, 01 Sep 2024 00:00:00 +0000

Background: Premna serratifolia Linn. (PS) was studied for phytochemical properties and antioxidant activity, as well as for its ability to inhibit the enzyme Acetylcholinesterase (AchE) and dock with PS molecules. Materials and Methods: An LC-MS/MS and GC-MS analysis of dried leaf extracts was performed for phytochemical identification, radical scavenging assays, and enzyme-based AchE inhibitory activity, as well as structurally-based molecular design of AchE inhibitors. Results: PS leaf extract was screened using phytochemical methods such as GC-MS and LC-MS/MS to identify its active constituents. DPPH radical (alcoholic 49.94 μg/mL and hydroalcoholic 49.89 μg/mL) was significantly inhibited by PS extracts at 20 and 40 μg/mL, as were their respective IC50 values. PS-alcoholic and PS-hydro alcoholic leaf extracts inhibited AchE by 49.45 μg/mL and 49.56 μg/mL, respectively. Conclusion: PS inhibits AchE and in vitro radicals scavenges, demonstrating its potential for reversing cholinergic deficits in Alzheimer's patients.

Evaluation of Lemon Peel Extract as Hepatoprotective Agent against Paracetamol-Induced Liver Toxicity: Insights from Biochemical Studies

Radhe Prasad Charmkar, Nazneen Dubey, Aditya Ganeshpurkar — Sun, 01 Sep 2024 00:00:00 +0000

Background: The liver serves as a vital organ in metabolic processes and detoxification, making it susceptible to damage induced by xenobiotics such as drugs. Paracetamol overdose is a common cause of hepatotoxicity. Traditional medicine has long explored botanical sources for hepatoprotective agents, highlighting the potential of natural compounds in mitigating liver damage. Lemon peel, rich in flavonoids with antioxidant properties, presents a promising candidate for hepatoprotection. Materials and Methods: This study aimed to investigate the hepatoprotective effects of lemon peel extract on paracetamol-induced liver toxicity in rats. The extract was prepared through standardized extraction procedures and its dose was selected based on previous studies. Wistar rats were divided into five groups and subjected to various treatments, including paracetamol overdose with or without lemon peel extract supplementation. Biochemical parameters indicative of liver function, such as serum levels of AST, ALT, ALP and bilirubin, were measured following treatment protocols. Results: Administration of paracetamol alone induced significant elevation in serum levels of AST, ALT, ALP and bilirubin, reflecting hepatocellular damage. However, co-administration of lemon peel extract with paracetamol resulted in reduced levels of these biochemical markers compared to the paracetamol-only group. The decrease in enzyme levels suggests potential hepatoprotective effects of lemon peel extract. Conclusion: Lemon peel extract demonstrated hepatoprotective effects against paracetamol-induced liver toxicity in rats, as evidenced by the attenuation of biochemical markers indicative of liver damage. These findings highlight the therapeutic potential of lemon peel extract as a natural remedy for protecting liver health and mitigating the adverse effects of hepatotoxic agents.

Protective Effects of Tinospora cordifolia on Cyclophosphamide-induced Nephrotoxicity in Wistar Rats

Ram Naresh Yadav, Aditya Ganeshpurkar, Nazneen Dubey — Sun, 01 Sep 2024 00:00:00 +0000

Background: Nephrotoxicity induced by drugs is a common cause of renal failure, particularly with agents like cyclophosphamide used in cancer treatment. Natural antioxidants found in plants offer diverse therapeutic benefits. Tinospora cordifolia, a medicinal plant known for its hepatoprotective, diuretic, carminative, digestive, and anti-helminthic properties, was investigated for its potential to counter cyclophosphamide-induced kidney damage in rats. Materials and Methods: Extracts were prepared from dried Tinospora powder, rich in flavonoids, polyphenolics, and alkaloids. Rats were divided into control and treatment groups, with varying doses of the Tinospora extract alongside cyclophosphamide. The blood sample was evaluated for creatinine, urea and BUN. Results: Treatment with the extract, particularly at 400 mg/kg, significantly reduced creatinine levels, as well as serum urea and blood urea nitrogen (p<0.01). These results highlight Tinospora cordifolia's nephroprotective potential, attributed to its flavonoid and polyphenol content. Conclusion: This study underscores the promise of plant-derived compounds in mitigating drug-induced kidney damage, suggesting Tinospora cordifolia as a potential adjunct therapy to preserve renal function during chemotherapy. Further research is needed to elucidate mechanisms and validate these findings for clinical application.

Comparative Hypertestosteronemic Effects of the Erythropoietin and the U-74389G

Sun, 01 Sep 2024 00:00:00 +0000

Background: This study is to find out in which direction two antioxidant promising molecules, the erythropoietin and the U-74389G, affect serum Testosterone (T) levels and what the magnitude of this alteration is. The posttreatment effects on serum Testosterone (T) levels were calculated, separately by each drug and afterwards a comparative calculation was following. Objectives: The estimation was extracted by the results of the 2 previous studies, each of which had estimated a certain influence, after the respective drug administration in an induced Ischemia-Reperfusion (IR) rat experiment. Materials and Methods: The 2 temporal experimental endpoints at which the serum T levels were measured were the 60th reperfusion min (for the 3 groups A, C and E) as well the 120th reperfusion min (for the other 3 groups B, D and F). Especially, the groups A and B were the placebo ones, the groups C and D were the post Epo; whereas the groups E and F were the post L administration. Results: The first previous study of Epo presented a non-significant hypertestosteronemic effect by 0.276%±0.272% (p-value=0.3006). Similarly, the second previous study of U-74389G presented also a non-significant hypertestosteronemic effect by 0.111%±0.179% (p-value=0.5245). The results of these 2 studies co-calculated as belonging to the same experimental setting, provided the outcome of L being just by 0.4046004 [0.4035126 - 0.4056911] less hypertestoteronemic than Epo (p-value=0.0000). Conclusion: The intrinsic antioxidant capacity of U-74389G ascribes just 0.4046004 [0.4035126 - 0.4056911] less hypertestoteronemic influence than Epo (p-value=0.0000).