Spergularia marina: a potential source of a novel calcium channel blocker with antihypertensive and diuretic activities.

OBJECTIVE: Spergularia marina (L.) Griseb. (S. marina) is a sub-cosmopolitan species used as traditional phytotherapy based on diverse biological activities. It is native and widespread in the northern hemisphere, though introduced also into the southern hemisphere. The extract of another species 'Spergularia purpurea' has been traditionally used in Morocco against various diseases and S. marina, itself, is a local popular food in South Korea. In this context, we evaluated the potential antihypertensive and diuretic effects of S. marina water and n-butanol extracts in L-NAME-induced hypertensive rats vs. the well-known diuretic, furosemide. MATERIALS AND METHODS: After toxicity studies, selected doses were administered orally daily for one week. Mean arterial blood pressure (MABP), water/electrolyte clearance, renal functions, and serum electrolytes were assessed. Vascular reactivity of isolated aortic rings was evaluated under different incubating settings against various antagonists to unravel the mechanism of action. RESULTS: Both extracts significantly reduced the MABP. Only, the n-butanol fraction exerted a significant aquaresis, increasing electrolyte free-water clearance with a significantly decreased urinary Na+, K+, and C- excretion. The water extract significantly augmented the ACh-induced relaxation and attenuated the NE-induced aortic rings' contractile response. It also exhibited a direct relaxant effect on the NE-precontracted rings with intact or denuded endothelium. Blocking the vascular calcium channels by preincubation with nifedipine prevented the S. marina-induced relaxation, denoting a calcium channel blocking activity. CONCLUSIONS: The vasorelaxant and the differential diuretic effects of both extracts introduce S. marina as a potential novel antihypertensive agent with calcium channel blocking activity. To enrich cardiovascular therapeutics, human studies to confirm the efficacy and safety of S. marina in hypertension are warranted. GRAPHICAL ABSTRACT: https://www.europeanreview.org/wp/wp-content/uploads/Graphical-abstract.jpg.

ß2-Adrenoceptor agonists as potential therapeutic drugs in diabetic peripheral neuropathy.

OBJECTIVES: the aim of the current study was to assess the effect of a ß2-adrenoceptor agonist; namely salbutamol, on hyperalgesic as well as nerve dysfunction components of diabetic peripheral neuropathy. MATERIAL AND METHODS: the present study was conducted on 60 male Wistar albino rats divided into six groups. Groups I and II were normal control rats injected by a single i.p. injection of normal saline and received 2% gum acacia (Group I) or salbutamol (Group II) for six weeks, starting one week following saline injection. Groups III-VI: rats that were rendered diabetic by a single i.p. injection of STZ and received either 2% gum acacia, salbutamol, salbutamol and propranolol or salbutamol and atenolol, respectively daily orally for six weeks, starting one week following STZ injection. RESULTS: vehicle-treated diabetic rats exhibited: significant sciatic nerve dysfunction in the form of significantly prolonged distal latency and significantly decreased maximum peak and peak to peak amplitude of compound muscular action potential, significant thermal and mechanical hyperalgesia evidenced by significant decrease in hot plate latency, tail-flick latency and vocalization threshold, respectively. Salbutamol administration improved nerve dysfunction as well as thermal and mechanical hyperalgesia. These effects of salbutamol are most likely mediated by ß2-adrenoceptors evidenced by significant abolishment of salbutamol effects after administration of the non-selective rather than the selective beta blockers; propranolol and atenolol, respectively. CONCLUSIONS: chronic administration of salbutamol could ameliorate DPN, an effect which is most likely mediated by ß2-adrenoceptors.

Investigating the role of zinc in a rat model of epilepsy.

AIMS: The aim of the present study was to investigate the role of zinc (Zn) in pilocarpine-induced seizures and its interrelation with an antiepileptic drug, namely, valproic acid. METHODOLOGY: The study was carried out on 110 male Wistar albino rats that were divided into the following groups: Group I, control rats that received intraperitoneal (i.p.) saline vehicle; Groups II-V received Zn in a medium dose, Zn in a high dose, valproic acid in a therapeutic dose, as well as a combination of valproic acid with medium dose Zn, respectively, for 3 weeks before saline injection, Group VI received i.p. pilocarpine to induce seizures; Groups VII-XI received Zn in a medium dose, Zn in a high dose, valproic acid in a therapeutic dose, a combination of therapeutic dose of valproic acid with medium dose Zn, as well as a combination of subeffective dose of valproic acid with medium dose of Zn, respectively, for 3 weeks before pilocarpine injection. The seizure's latency and severity for each rat was recorded. Blood and brain hippocampal samples were collected for determination of serum neuron specific enolase (NSE), hippocampal Zn, interleukin-1 beta concentrations as well as hippocampal superoxide dismutase and caspase-3 activities. RESULTS: The results of the current study demonstrated that pretreatment with high dose of Zn exacerbated pilocarpine-induced seizures. Whereas, a medium dose of Zn and valproic acid either alone or in combination reduced the severity of pilocarpine-induced limbic seizures and increased the latency to attain the forelimb clonus. Also both drugs, either alone or in combination, ameliorated all studied biochemical parameters with the exception of hippocampal Zn concentration, which was only significantly increased by pretreatment with Zn, either alone or in combination with valproic acid. CONCLUSIONS: The present study highlights the antiepileptic role that could be played by Zn, when given in appropriate doses.