Coronavirus disease 2019 (COVID-19) is a virulent viral disease that has now become a public health emergency of global significance and still without an approved treatment regimen or cure. In the absence of curative drugs and with vaccines development still in progress, alternative approaches to stem the tide of the pandemic are being considered. The potential of a phytotherapeutic approach in the management of the dreaded disease has gained attention, especially in developing countries, with several claims of the development of anti-COVID-19 herbal formulations. This is a plausible approach especially with the increasing acceptance of herbal medicine in both alternative and orthodox medical practices worldwide. Also, the established efficacy of herbal remedies in the treatment of numerous viral diseases including those caused by coronaviruses, as well as diseases with symptoms associated with COVID-19, presents a valid case for serious consideration of herbal medicine in the treatment of COVID-19. However, there are legitimate concerns and daunting challenges with the use of herbs and herbal products. These include issues of quality control, unethical production practice, inadequate information on the composition, use and mechanisms, weak regulatory policies, herb-drug interactions and adverse reactions, and the tendency for abuse. This review discusses the feasibility of intervention with herbal medicine in the COVID-19 pandemic and the need to take proactive measures to protect public health by improving the quality and safety of herbal medicine deployed to combat the disease.

Background: Parkia biglobosa leaf has popular ethnomedicinal use in tropical Africa. However, little is known about its molecular biological effects. This study sought to investigate the in vitro antioxidant activity, angiotensin-Iconverting enzyme (ACE) inhibition and effects of aqueous-methanolic extract of P. biglobosa leaf (PBE) on mitochondrial membrane potential and reactive oxygen species (ROS) generation. Methods: Antioxidant activity was determined by extract's DPPH .(1,1-diphenyl-2-picrylhydrazyl radical), ABTS .+ [2,2′-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) diammonium salt radical cation] scavenging ability, reducing property and propensity to inhibit lipid peroxidation induced by prooxidants (FeSO 4 /sodium nitroprusside, SNP) in isolated rat tissue preparations. Determination of angiotensin-converting enzyme (ACE) inhibition was based on the hydrolysis of N-hippuryl-His-Leu hydrate (HHL) by the enzyme. Subsequently, the effects of PBE on toxicant-induced mitochondrial ROS formation and basal membrane potential (ΔΨm) were determined by 2′, 7′-dichlorodihydrofluorescin (DCFH) oxidation and safranine fluorescence respectively. Results: PBE significantly reduced ferric ions (P < 0.001), scavenged DPPH (EC 50 = 98.33 ± 1.0 μg/mL) and ABTS (EC 50 = 45.30 ± 0.1) radicals, with moderate Fe 2+ -chelating effect (40%). In rat liver and brain homogenates respectively, PBE prevented membrane peroxidation induced by FeSO 4 (EC 50 : 75.87 ± 2.1 μg/mL and 89.34 ± 2.5 μg/mL) and SNP (EC 50 : 28.10 ± 1.6 μg/mL and 17.25 ± 0.78 μg/mL). The extract's inhibition of ACE (IC 50 = 51.30 ± 5.1 μg/mL) and mild depolarization of isolated liver mitochondria membrane potential were concentration-dependent. Finally, PBE was more effective than catechin in attenuating calcium and SNP-induced surge in mitochondrial ROS generation. Conclusion: Parkia biglobosa leaf exhibits considerable ACE inhibitory effect, antioxidant activity and affects mitochondrial redox chemistry. These present findings also justify the ethnobotanical applications of the plant in the indigenous system of medicine.

Aims: To investigate the antioxidant activities and effects of free phenols (FPPB) and bound phenols (BPPB) of Parkia biglobosa leaves on some enzymes of neuro-cardiovascular relevance.Methods and Results: HPLC-DAD fingerprinting of FPPB and BPPB, and the antihemolytic, radical (1,1-diphenyl-2 picrylhydrazyl, DPPH; 2,2-azino-bis(3-ethylbenzthiazoline-6-sulphonic acid), ABTS) scavenging and ferric reducing antioxidant properties of extracts, were assessed. In addition, the effects of the phenolics on angiotensin-1-converting enzyme (ACE), cerebral acetylcholinesterase/butyrylcholinesterase (AChE/BuChE), and Na + /K + ATPase were determined in vitro. FPPB was more potent than BPPB in terms of ABTS (EC 50 :4.06 ± 0.3 vs 24.07 ± 2.1 μg/mL) and DPPH (EC 50 :3.82 ± 0.2 vs 10.22 ± 0.1 μg/mL) radicals scavenged, respectively. The free phenolic extract was a better DPPH . scavenger than ascorbic acid (EC 50 = 12.58 ± 0.4 μg/mL; DPPH reference) and compared well withTrolox (EC 50 :4.44 ± 0.08 μg/mL; ABTS reference). The anti-hemolytic effect of FPPB (36%) and BPPB (53%) was highest at 15 μg/mL but lower than that recorded for ascorbic acid (67% at 10 μg/mL). Even though FPPB (IC 50 = 15.35 ± 4.0 μg/mL) and BPPB (IC 50 = 46.85 ± 3.3 μg/ mL) showed considerably lower ACE-inhibitory effect than ramipril (IC 50 :0.173 ± 0.04 μg/mL), both extracts demonstrated dose-dependent, significant (p < 0.01/p < 0.05) inhibition of the enzyme. FPPB increased cerebral Na+/K+ATPase activity but neither phenolic extract affects cerebral AChE/BuChE activities. HPLC-DAD revealed catechin, caffeic acid, and quercetin, respectively, as the major phenolics (mg/g) in FPPB (29.85, 30.29, and 17.10) and BPPB (32.70, 30.51, and 19.25). Conclusion:The effects of P biglobosa on ACE and cerebral ATPase are related to its constituent phenolics. ACE inhibition could be an important mechanism underlying the documented hypotensive effect of the plant. ----------------------------------------------This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Neem (Azadirachta indica) plant components are popularly applied in ethnomedicine for the management of numerous diseases. The current study aimed to assess the anti-diabetic potential and mechanism of neem seed oil (NSO) in a rodent model of type 2 diabetes mellitus induced by a chronic high-fat diet and a single low-dose of streptozotocin. Diabetic animals (blood glucose levels ≥ 220 mg/dL) were post-treated (orally) with NSO (200 and 400 mg/kg) or the standard drug, metformin (150 mg/kg), for 30 days. Two other groups served as the negative and positive controls. NSO significantly (p<0.05) reversed diabetes-induced hyperglycemia, impaired glucose tolerance, dyslipidemia, and oxido-inflammatory imbalances typified by alterations in the NADH/NAD+ ratio (p<0.001), elevations in the levels of C-reactive protein, 4-hydroxynonenal, malondialdehyde, and pro-inflammatory cytokines (TNF-α and Il-1β), and reductions in endogenous antioxidant enzymes. Furthermore, gene expression of inflammatory cytokines and glycogen synthase kinase 3 beta (GSK-3β) was upregulated in the hepatic and pancreatic tissues of NSO-treated animals. The protective effect of NSO was corroborated by the histological assessment of the pancreatic tissue. The results revealed that the anti-diabetic potential of NSO proceeded through its hypolipidemic activity and modulation of redox and inflammatory signaling events in the hepatic and pancreatic tissues.

Aim: Parinari curatellifolia seed flavonoid extract (PFE) and crude methanol extract (PME) were investigated for their effects on Triton X-100 (TRT; 200 mg/kg i.p.)-induced dyslipidemia in rats. Methods: Experimentally induced hyperlipidemic and un-induced, normal rats were treated with nicotinic acid (300 mg/kg), PFE (20, 25, 30 mg/kg) or PME (100, 150 mg/kg) once daily by gavage for 10 days, following which the biochemistry and histology of the heart, aorta and sera were analyzed. Results: The seed extracts produced slight decreases in serum activities of the cardiac markers creatine kinase and lactate dehydrogenase, and did not perturb the cardiac antioxidant status of normal rats. TRT promoted cardiac oxidative stress, decreased high-density lipoprotein cholesterol (75%, P < 0.001) and increased total cholesterol (TC; 97%, P < 0.001), triglycerides (138%, P < 0.001), low-density lipoprotein cholesterol (LDL-c; 281%, P < 0.001), coronary risk index (CRI; sixfold) and atherogenic risk index (ARI; 13-fold). PFE (20 mg/kg) and PME (150 mg/kg), respectively, restored cardiac antioxidant status and significantly ameliorated the astronomical changes produced by TRT as regards TC (56% and 31%), triglycerides (70% and 66%), LDL-c (96% and 46%), CRI (92% and 78%) and ARI (99% and 83%), with relatively better efficacy than the reference compound, nicotinic acid (P < 0.01/0.001). In addition, improved heart and aortic histological architecture was observed in rats treated with both extracts. On high-performance liquid chromatography screening, kaempferol, rutin, and quercitrin were identified as some of the active phytochemicals in PFE. Conclusion: P. curatellifolia seed flavonoids have remarkable anti-hyperlipidemic and anti-atherogenic effects in acute dyslipidemia caused by TRT.

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