Why honey is effective as a medicine. 1. Its use in modern medicine

Honey has been used as a medicine for thousands of years and its curative properties are well documented. However, modern medicine turned its back on honey and it is only now, with the advent of multi-resistant bacteria, that the antibiotic properties of honey are being rediscovered

Honey potentiates the gastric protection effects of sucralfate against ammonia-induced gastric lesions in rats

Background: Natural honey is widely used all over the world as a complementary and alternative medicine in various disorders including gastrointestinal lesions. Aim: To evaluate the effects of combination of low dosage of honey (0.312g/kg) and sucralfate (0.125 or 0.250 g /kg) on gastric protection and to determine any potentiating interactions between them against ammonia-induced gastric lesions in rats. Material and Methods: Twenty-four hours fasted rats were given I ml of ammonium hydroxide 1 % intragastrically and they were killed one hour later under deep ether anesthesia. The gastric lesion index was calculated according to the method of Takaishi et al 1998. Non protein sulthydryls level was determined spectrophotometrically as described by Sedlak and Lindsay 1968. Results: Administration of ammonium hydroxide produced red and black linear lesions and significant depletion of gastric nonprotein sulthydryls level. Oral administration of honey (0.312g/kg) or sucralfate (0.125 and 0.250g/kg) 30min before ammonium hydroxide reduced the severity of gastric mucosal lesions by 1 I or 18 and 42 % respectively, and has shown the changes in nonprotein sulfhydryls level induced by ammonium hydroxide. Furthermore, pretreatment with a combination of a low dose of honey (0.312g /kg) and sucralfate (0.125g or 0.250g/kg) afforded significantly greater protection (58 and 77 %) than that obtained with either of them administered alone. Conclusion: The present results suggest potentiation of gastric protection effect of sucralfate by honey and this may have a clinical value in the treatment of peptic ulcer diseases in Helicobacter pylori positive patient

Vasorelaxant effect of nitric oxide releasing steroidal and nonsteroidal anti-inflammatory drugs

1. The effect of several nitric oxide releasing-non-steroidal anti-inflammatory drugs (NO-NSAID) and nitroprednisolone on blood vessel relaxation in vitro and in vivo was studied. Nitroflurbiprofen (NOF; EC(50), 688.8±93.8 μM), nitroaspirin (NOA; EC(50), 57.9±6.5 μM), nitroparacetamol (NOPARA; EC(50), 71.5±14.6 μM) and nitroprednisolone (EC(50), 15.1±1.4 μM) caused concentration-related relaxation of noradrenaline (NA)-contracted rat aortic rings. All NO releasing compounds tested were approximately three orders of magnitude less potent than sodium nitroprusside (SNP, EC(50), 35.7±3.5 nM). 2. The vasorelaxant effect of NOF and NOPARA in the rat aorta was potentiated by zaprinast (5 μM) and reduced by ODQ (5 μM). Flurbiprofen and paracetamol (100 μM) caused minimal (<10%) relaxation of the rat aorta and did not affect the response to SNP. The effect of NOF was unchanged in the presence of L-NAME (100 μM; EC(30), 181.8±35.1 μM cf. EC(30), 125.1±17.0 μM, P>0.05) but increased by removal of the endothelium (EC(30), 164.3±26.3 μM cf. EC(50), 688.8±93.8 μM, P<0.05). 3. NOF (0.1–50 μM) produced a small but not concentration-related vasodilation of the NA-preconstricted (i.e. ‘high tone') perfused rat mesentery preparation (cf. SNP, EC(30), 4.4±0.7 μM). In contrast, NOF (1–100 μM) produced concentration-related vasodilation of the ‘high tone' perfused rat kidney with an EC(50) of 33.1±4.4 μM. 4. Neither NOF (74 mg kg(−1), i.p.) nor NOA (91.9 mg kg(−1), i.p.) nor equimolar doses of flurbiprofen (50 mg kg(−1), i.p.) or aspirin (50 mg kg(−1), i.p.) affected mean arterial blood pressure (MAP) or heart rate (HR) of pentobarbitone-anaesthetized rats over a 1 h period. 5. NO-NSAID relax blood vessels in vitro by an NO-dependent mechanism. The absolute vasorelaxant effect of NO releasing drug varies greatly with the choice of compound and between blood vessel preparations

Role of oxygen-derived free radicals on gastric mucosal injury induced by ischemia-reperfusion

A free radical is an unstable and highly-reactive chemical species capable of independent existence that contained one or more unpaired electrons in its outer orbital. A number of oxygen-derived free radicals (ODFRs) have been identified. However, superoxide (O-2) and hydroxyl (OHFNx01) radicals are extensively studied. The univalent reduc-tion of oxygen to water produces a number of highly-reactive chemical intermediates such as O-2 and OHFNx01, which are commonly-known as oxygen-derived free radicals. ODFRS may be formed from several sources as follows: a) mitochondrial cytochrome oxidase, b) xanthine oxidase, c) neutrophils and d) transitional metals. There are several important defense mechanisms to limit or to prevent the damage caused by excessive ODFRs activity. These antioxidant defenses can be divided into a) enzymatic defense mechanisms such as : superoxide dismutase (SOD): catalase: selenium-containing glutathione peroxidase and b) non-enzymatic defense mechanisms including: alpha-tocopherol; ascorbic acid; glutathione and any sulfhydryl-containing compounds

A comparison of the effect of nitroparacetamol and paracetamol on liver injury

Paracetamol (5 mmol kg(−1), i.p.) caused liver damage in rats as indicated by increased plasma aspartate aminotransferase (AST), alanine aminotransferase (ALT) and glutamate dehydrogenase (GDH) activities. No change in plasma bilirubin or creatinine was noted. An equimolar dose of nitroparacetamol (a nitric oxide (NO)-releasing derivative of paracetamol) did not alter plasma levels of any of the markers of liver/kidney damage. No difference in plasma or liver paracetamol was apparent in animals injected with paracetamol or nitroparacetamol. These results indicate that NO released from nitroparacetamol exhibits hepatoprotective activity in these animals and suggest that nitroparacetamol may therefore be considered as a safer alternative to paracetamol in the clinic

Prevalence, knowledge and attitudes toward herbal medication use by Saudi women in the central region during pregnancy, during labor and after delivery

Abstract Background Herbal medication usage is prevalent in both developing and developed countries. The low level of awareness of the possible dangers of some herbs during pregnancy increases the risk of unwarranted sequelae. This manuscript describes the first study of herbal medication use among pregnant women in Saudi Arabia. It aims to determine the prevalence of herbal medication use during pregnancy, during labor and after delivery in the central region of Saudi Arabia. Methods A cross-sectional descriptive study was conducted over a 5-month period from May 15 to October 15, 2016. A self-administered questionnaire was distributed at 4 main hospitals and 3 primary care centers in Riyadh and Al Kharj. Data from 612 participants were collected and analyzed. Descriptive statistics in the form of frequency and percentage were determined, and Chi-squared tests were performed. Results Of the 612 participants, 25.3%, 33.7% and 48.9% used herbs during pregnancy, during labor, and after delivery, respectively. The primary motives for using herbal medication during pregnancy, during labor and after delivery were to boost general health, ease and accelerate labor and clean the womb, respectively. There was a significant association between use during pregnancy and prior use (P = 0.001). Most pregnant women used herbs based on advice from family and friends (52.9%). Only 40.7% of pregnant women disclosed their herbal use to their doctors. Conclusion The prevalence of herbal medication use among pregnant Saudi women in Riyadh and Al Kharj is relatively high. Doctors should be aware of evidence regarding the potential benefits or harm of herbal medication use during pregnancy

Selenium protects against ischemia-reperfusion- induced gastric lesions in rats

Recent studies have shown that selenium afforded protection against ethanol and stress-induced gastric lesions in rats. The present study was undertaken to investigate the effect of selenium on ischemia-reperfusion-induced gastric injuries in which rats were subjected to 30 minutes of ischemia in the presence of 100 mM HCI and a reperfusion for 60 minutes duration. Intraluminal bleeding was assessed macroscopically and gastric lesions were graded microscopically under an inverted microscope. Nonprotein sulphydryl levels were measured spectrophotometrically. The severity of gastric lesions, intraluminal bleeding as well as the depletion of nonprotein sulphydryls during the reperfusion periods was significantly different from that of control. Pretreatment with selenium (0.125-2.0 mg/kg, intraperitoneally) 30 minutes before the ischemia-reperfusion, dose-dependently attenuated the gastric lesions, reduced the severity of intraluminal bleeding and prevented the depletion of nonprotein sulphydryls in the stomach. These results suggest that the gastric protection effect of selenium may be due to its antioxidant properties. Furthermore, endogenous nonprotein sulphydryls may play a significant role in the protective mechanisms of selenium