Quercetin is a phenolic flavonol compound with established antioxidant, anti-inflammatory, and immuno-stimulant properties. Recent studies demonstrate the potential of quercetin against COVID-19. This article highlighted the prophylactic/therapeutic potential of quercetin against COVID-19 in view of its clinical studies, inventions, and patents. The literature for the subject matter was collected utilizing different databases, including PubMed, Sci-Finder, Espacenet, Patentscope, and USPTO. Clinical studies expose the potential of quercetin monotherapy, and also its combination therapy with other compounds, including zinc, vitamin C, curcumin, vitamin D3, masitinib, hydroxychloroquine, azithromycin, and ivermectin. The patent literature also examines claims that quercetin containing nutraceuticals, pharmaceuticals, and dietary supplements, alone or in combination with other drugs/compounds, including favipiravir, remdesivir, molnupiravir, navitoclax, dasatinib, disulfiram, rucaparib, tamarixin, iota-carrageenan, and various herbal extracts (aloe, poria, rosemary, and sphagnum) has potential for use against COVID-19. The literature reveals that quercetin exhibits anti-COVID-19 activity because of its inhibitory effect on the expression of the human ACE2 receptors and the enzymes of SARS-CoV-2 (MPro, PLPro, and RdRp). The USFDA designated quercetin as a “Generally Recognized as Safe” substance for use in the food and beverage industries. It is also an inexpensive and readily available compound. These facts increase the possibility and foreseeability of making novel and economical drug combinations containing quercetin to prevent/treat COVID-19. Quercetin is an acidic compound and shows metabolic interaction with some antivirals, antibiotics, and anti-inflammatory agents. Therefore, the physicochemical and metabolic drug interactions between quercetin and the combined drugs/compounds must be better understood before developing new compositions.
Due to the increasing problem of drug resistance, new and improved medicines are required. Natural products and biotherapeutics offer a vast resource for new drugs; however, challenges, including the cost and time taken for traditional drug discovery processes and the subsequent lack of investment from the pharmaceutical industry, are associated with these areas. New techniques are producing compounds with appropriate activity at a faster rate. While the formulation of these combined with drug-delivery systems offers a promising approach for expanding the drug developments available to modern medicine. Here, various classes of drug-delivery systems are described and the advantages they bring to small molecule and biotherapeutic targeting are highlighted. This is an attractive approach to the pharmaceutical industry and the rising trend in research in this area is examined in brief. New medicines are constantly being developed or repurposed, aimed at curing or preventing diseases or conditions where therapeutic product availability is lacking, or to reduce side effects, improve quality of life, reduce the burden on the cost of healthcare systems, while significantly extending patients' lives. However, drug discovery, research and development (R&D) can be an extensive process lasting over 7-10 years, with an average cost of $2.6 billion for each successful drug that reaches the market [1]. These substantial cost and time factors originate from the scientific, technical and regulatory challenges that are needed to fully understand the drug mechanisms of action and physiological interactions for complex diseases at molecular level. Achieving viable commercial success subsequently
Papaver decaisnei (P. decaisnei) has been used as folkloric medicine for many health issues including gastric problems. The current study investigates the gastroprotective roles of P. decaisnei against ethanol-induced ulcers in rodents. Sprague Dawley rats (30) were separated into five groups: the normal group (G1) and the ulcer control group (G2) were orally administered 0.5% carboxymethylcellulose (CMC); the reference group (G3) was administered 20 mg/kg of Omeprazole; two experimental groups were fed with 200 mg/kg (G4) and 400 mg/kg (G5) of the P. decaisnei extract (PDE), respectively. Next, the rats were given absolute ethanol and sacrificed for the analysis of the gastric mucosal injury through microscopic, enzymatic, histologic, and immunohistochemistry assays. The ulcer controls showed significant superficial hemorrhagic gastric mucosal lesions, with a decreased gastric wall mucus and edema production, whereas fewer were found for the reference and plant-treated rats. Furthermore, the PDE pre-treated rats had a significantly reduced the periodic acid-Schiff (PAS) staining intensity, produced the upregulation of the HSP70 protein, and the downregulation of the Bax protein expressions in the stomach epithelium. P. decaisnei displayed a significant role in the upregulation of endogenous antioxidant enzymes (SOD, CAT, and PGE2), significantly reduced malondialdehyde (MDA), TNF-a, IL-6, and upraised the IL-10 levels. Based on the positive impacts, the PDE can be proposed as the protective/treatment agent against gastric ulcers and stomach lesions.
Ethnopharmacological relevance Since ancient times, herbal medicines have been applied in the treatment of cancer. Tea, derivative from the dried leaves of Camellia sinensis (L.) Kuntze plant is the most popular beverage globally after water and is available in various forms. Green tea has been expansively investigated for its beneficial properties of cancer prevention and therapy. The goal of the research: The current study was conducted to evaluate the hepaprotective character of methanolic green tea extract and its mechanism of action contrary to thioacetamide (TAA)-produced liver fibrosis of Sprague Dawley rats. Materials and Methods Thirty rodents were equally placed in 5 clusters including normal control, TAA group as a positive control, silymarin as standard drug control, and treatment groups consisting of high dose and a low dose Camellia sinensis. Rats in experimental clusters by mouth fed with C. sinensis at 250 mg/kg or 500 mg/kg daily for 2 months. After 60 days, all rats were sacrificed. Blood specimens were gathered for liver biochemical examination. Livers of all groups were dissected out and subjected to histopathological examination through the Hematoxylin and Eosin stain, Masson trichrome, and immunohistochemistry stains (PCNA). Liver tissue homogenate was also analyzed for antioxidant activity parameters. Results Gross morphological examination showed a regular liver architecture in C. sinensis fed collections compared to the TAA sets. Histology of rat’s liver fed with C. sinensis showed an important decrease in the liver index with hepatic cells propagation, mild cellular injury, and immunostaining showed significant down-expression of proliferating cell nuclear antigen (PCNA). TAA produced liver fibrosis through a significant increase in serum alanine transferase, aspartate aminotransferase, alkaline phosphatase, and bilirubin. Total protein and albumin also decreased in the TAA group. Moreover, the reduction of antioxidant enzyme activity including superoxide dismutase and catalase as well as the increase in malondialdehyde was detected in the TAA control group. Meanwhile, an abnormal level of liver biochemical parameters was restored closer to the normal levels in serum of the C. sinensis-fed clusters. In addition, C. sinensis fed assemblies showed elevated antioxidative enzymes activity with a reduction in malondialdehyde level comparable to the levels in silymarin-treated rats. Conclusions Green tea potentially inhibited the progression of liver cirrhosis, down -regulation of PCNA proliferation, prevented oxidation of hepatocytes, recovered SOD and CAT enzymes, condensed MDA and reduced cellular inflammation.
This research in vivo assessed the impact of the ethanolic extract of Annona muricata (A. muricata) on the histopathology, immunohistochemistry, and biochemistry of thioacetamide (TAA)-induced liver cirrhosis in Sprague Dawley rats. The rats, gavaged precisely with two doses of A. muricata (250 mg/kg and 500 mg/kg) with TAA, presented a substantial reduction in the liver index and hepatocyte propagation, with much lower cell injury. These groups showed meaningfully down-regulated proliferating cell nuclear antigen (PCNA) in the liver and spleen, α-smooth muscle actin (α-SMA), and transforming growth factor-beta 1 (TGF-β1) in liver parenchymal tissue. The liver homogenate displayed enhanced antioxidant enzymes, superoxide dismutase (SOD) and catalase (CAT) activity, along with a decrease in malondialdehyde (MDA) levels. The serum levels of bilirubin, total protein, albumin, and liver enzymes alkaline phosphatase (ALP), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) were returned to normal and were similar to that of the normal control and silymarin with TAA-treated groups. Oral acute toxicity revealed no evidence of any toxic symbols or mortality in rats, indicating the safety of A. muricata. Therefore, the normal microanatomy of hepatocytes, the clampdown of PCNA, α-SMA, TGF-β, improved antioxidant enzymes (SOD and CAT), and condensed MDA with repairs of liver biomarkers validate the hepatoprotective effect of A. muricata.
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