Factors hindering the implementation of clinical pharmacy practice in Egyptian hospitals.

Background: The direction toward incorporating clinical pharmacy services is increasing worldwide but there are many barriers that hinder its implementation in many countries. The types of barriers vary among countries according to their culture, population, education & economic status. Objective: This study aims to investigate factors hindering the implementation of clinical pharmacy practice in Egyptian hospitals. Methods: Hundred hospital pharmacists working in various reputable hospitals in Egypt participated in a descriptive cross-sectional survey designed as a questionnaire representing the main factors previously reported in the literature to hinder clinical pharmacy implementation in different countries around the world. Cronbach alpha was calculated to test the reliability of the questionnaire. Likert plot was used to graphically present the participants' responses. Results: The most significant factors that participants reported to hinder the implementation of clinical pharmacy practice in Egyptian hospitals were the lack of clear career path, financial resources, and leadership support. The percentage of participants who agreed that such factors were key players in hindering the implementation of clinical pharmacy practice was 76%, 74%, and 57% respectively. Conclusion: A number of factors were found to impede clinical pharmacy implementation in Egyptian hospitals. Taking corrective measures to resolve such hindrances should ensure proper hospital pharmacy practice and should positively reflect on patient healthcare services provided at the national level.

Factors Hindering the Implementation of Clinical Pharmacy Practice in Egyptian Hospitals

Background: The direction toward incorporating clinical pharmacy services is increasing worldwide but there are many barriers that hinder its implementation in many countries. The types of barriers vary among countries according to their culture, population, education & economic status. Objective: This study aims to investigate factors hindering the implementation of clinical pharmacy practice in Egyptian hospitals. Methods: Hundred hospital pharmacists working in various reputable hospitals in Egypt participated in a descriptive cross-sectional survey designed as a questionnaire representing the main factors previously reported in the literature to hinder clinical pharmacy implementation in different countries around the world. Cronbach alpha was calculated to test the reliability of the questionnaire. Likert plot was used to graphically present the participants’ responses. Results: The most significant factors that participants reported to hinder the implementation of clinical pharmacy practice in Egyptian hospitals were the lack of clear career path, financial resources, and leadership support. The percentage of participants who agreed that such factors were key players in hindering the implementation of clinical pharmacy practice was 76%, 74%, and 57% respectively. Conclusion: A number of factors were found to impede clinical pharmacy implementation in Egyptian hospitals. Taking corrective measures to resolve such hindrances should ensure proper hospital pharmacy practice and should positively reflect on patient healthcare services provided at the national level. (AU)

Potential value of pharmacological agents acting on toll-like receptor (TLR) 7 and/or TLR8 in COVID-19.

The COVID-19 pandemic is an ongoing global pandemic of coronavirus disease 2019 as an atypical type of viral pneumonia caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Many potential pharmacotherapies are currently being investigated against this disease. This article points to and justifies, the importance of investigating the potential therapeutic value of pharmacological agents acting on Toll-like Receptor (TLR) 7 and/or TLR8 as double-edged swords combating COVID-19. Induction of TLR7 and/or TLR8 may be investigated as a strategy to stimulate immunity and may be added to anti-COVID19 vaccines to cope with their current viral escape challenge. TLR7 stimulation may not only help viral clearance through Th1 antiviral responses but may also provide beneficial broncho- and vaso-dilatory, as well as, anti-inflammatory effects. Pharmacological compounds acting as TLR7 and/or TLR8 agonists may be of value if used by frontline healthcare workers with comorbidities who demonstrate mild symptoms of the disease. On the other hand, TLR7 and/or TLR8 antagonists may be used in combination with immune-modulatory/anti-inflammatory drugs in severe cases of the disease, with potential synergistic effects that could also help in reducing the doses of such therapies, and consequently their adverse effects.

Applicability of American College of Clinical Pharmacy (ACCP) competencies to clinical pharmacy practice in Egypt.

BACKGROUND: The American College of Clinical Pharmacy (ACCP) prepared clinical pharmacist competencies that have specific recommendations. Recently, many efforts to advance clinical pharmacy services in Egypt exist. The literature revealed that no country has assessed the extent of applicability of ACCP competencies in its current pharmacy practice setting. Egyptian pharmacists can provide feedback about applicability of such competencies in clinical pharmacy settings in Egypt. OBJECTIVE: The objective of this study was to investigate the extent to which ACCP competencies were implemented by Egyptian clinical pharmacists and therefore evaluate development of clinical pharmacy practice in Egypt. The study also investigated factors affecting the applicability of such competencies in the current clinical pharmacy practice setting in Egypt. METHODS: Four hundred and ninety-five randomly selected clinical pharmacists from several hospitals were invited to participate in a cross sectional survey using a self-administered validated questionnaire composed of 31 questions classified into six domains. This questionnaire was designed to determine the pharmacists' perception about applicability of ACCP competencies to clinical pharmacy practice in Egypt. RESULTS: The response rate was 64% as 317 out of 495 pharmacists completed the questionnaire. These pharmacists were categorized according to age; gender; qualifications; years of previous work experience, years since BSc. and type of hospitals they are currently working at. Analysis of data revealed the professionalism domain to have the highest percentage of acceptance among pharmacists, while the system-based care & population health domain had the lowest percentage of acceptance. Results also showed that qualifications of participants did not affect their response in three domains; "Direct Patient Care", "Systems-based Care & Population Health" and "Continuing Professional Development" (p=0.082, 0.081, 0.060), respectively. Nevertheless, qualifications of participants did affect their response in the other three domains; "Pharmacotherapy Knowledge", "Communication" and "Professionalism" (p<0.05). The age of pharmacists, gender, years of previous work experience, and graduation year did not affect their responses in all six domains. The type of hospital they are currently working at, though, affected their responses where, there was a highly statistically significant increase of the mean score of all domains among participants working at the NGOs/private hospitals compared to governmental hospitals (p<0.001). CONCLUSIONS: Egyptian pharmacists generally apply high percentage of ACCP competencies but the provided clinical pharmacy services need to be improved through applying the standards of best practice.

Ameliorative Effects of α-Tocopherol and/or Coenzyme Q10 on Phenytoin-Induced Cognitive Impairment in Rats: Role of VEGF and BDNF-TrkB-CREB Pathway.

Phenytoin is one of the most well-known antiepileptic drugs that cause cognitive impairment which is closely related to cAMP response element-binding protein (CREB) brain-derived neurotrophic factor (BDNF) signaling pathway. Moreover, vascular endothelial growth factor (VEGF), an endothelial growth factor, has a documented role in neurogenesis and neuronal survival and cognitive impairment. Therefore, this study aimed to investigate the influence of powerful antioxidants: α-Toc and CoQ10 alone or combined in the preservation of brain tissues and the maintenance of memory formation in phenytoin-induced cognitive impairment in rats. The following behavioral test novel object recognition and elevated plus maze were assessed after 14 days of treatment. Moreover, VEGF, BDNF, TrkB, and CREB gene expression levels in the hippocampus and prefrontal cortex were estimated using RT-PCR. Both α-Toc and CoQ10 alone or combined with phenytoin showed improvement in behavioral tests compared to phenytoin. Mechanistically, α-Toc and/or CoQ10 decreases the VEGF mRNA expression, while increases BDNF-TrKB-CREB mRNA levels in hippocampus and cortex of phenytoin-treated rats. Collectively, α-Toc and/or CoQ10 alleviated the phenytoin-induced cognitive impairment through suppressing oxidative damage. The underlying molecular mechanism of the treating compounds is related to the VEGF and enhancing BDNF-TrkB-CREB signaling pathway. Our study indicated the usefulness α-Toc or CoQ10 as an adjuvant to antiepileptic drugs with an advantage of preventing cognitive impairment and oxidative stress.

Molecular mechanisms of neuroprotective effect of adjuvant therapy with phenytoin in pentylenetetrazole-induced seizures: Impact on Sirt1/NRF2 signaling pathways.

Current anticonvulsant therapies are principally aimed at suppressing neuronal hyperexcitability to prevent or control the incidence of seizures. However, the role of oxidative stress processes in seizures led to the proposition that antioxidant compounds may be considered as promising candidates for limiting the progression of epilepsy. Accordingly, the aim of this study is to determine if coenzyme Q10 (CoQ10) and alpha-tocopherol (α-Toc) have a neuroprotective effect in rats against the observed oxidative stress and inflammation during seizures induced by pentylenetetrazole (PTZ) in rats, and to study their interactions with the conventional antiseizure drug phenytoin (PHT), either alone or in combination. Overall, the data revealed that α-Toc and CoQ10 supplementation can ameliorate PTZ-induced seizures and recommended that nuclear factor erythroid 2-related factor 2 (NRF2) and silencing information regulator 1 (Sirt1) signaling pathways may exemplify strategic molecular targets for seizure therapies. The results of the present study provide novel mechanistic insights regarding the protective effects of antioxidants and suggest an efficient therapeutic strategy to attenuate seizures. Additionally, concurrent supplementation of CoQ10 and α-Toc may be more effective than either antioxidant alone in decreasing inflammation and oxidative stress in both cortical and hippocampal tissues. Also, CoQ10 and α-Toc effectively reverse the PHT-mediated alterations in the brain antioxidant status when compared to PHT only.

Fingolimod interrupts the cross talk between estrogen metabolism and sphingolipid metabolism within prostate cancer cells.

Sphingolipids are critical regulators of tumor microenvironments and play an important role in estrogen-dependent cancers. Estrogen and estrogen metabolites were found to be involved in prostate cancer. Fingolimod (FTY720) is a sphingokinase-1 (SphK1) inhibitor with anticancer properties against various tumor cell types. Herein, we investigated the interference of FTY720 with the cross talk between sphingolipid metabolism and estrogen metabolism within prostate cancer cells. FTY720 showed cytotoxic antiproliferative effects against androgen-dependent and -independent prostate cancer cells with IC50 ranging from 3.0 ±â€¯0.3 to 6.8 ±â€¯1.7 µM. Exposure of prostate cancer cells to FTY720 resulted in a dramatic decrease in the concentration of estradiol, estrone, 4-hydroxyestradiol and 16α-hydroxyestrone compared to control cells. However, FTY720 significantly increased the concentration of 2-methoxyestrone and 2-methoxyestradiol within prostate cancer cells. This was mirrored by significant downregulating of the expression of estrogen and catechol estrogen-synthesizing enzymes (CYP19, CYP1A1 and CYP1B1) within prostate cancer cells. On the other hand, FTY720 significantly upregulated the expression of catechol estrogen-detoxifying enzyme (COMT). Additionally, FTY720 abolished estrogen-stimulated expression of ERα and basal expression of ERß within prostate cancer cells. Furthermore, FTY720 suppressed the expression of the ER-downstream regulated genes, CXCR4 and cyclin D1. Reciprocally, it was found that estradiol and catechol estrogens significantly induced the expression of SphK1 while methoxylated catechol estrogen suppressed its expression within prostate cancer cells in a dose-dependent manner. Current research has highlighted the hazardous influence of the estrogenic component to prostate cancer. We found that fingolimod (FTY720) could modulate the estrogenic micromilieu and interrupt its cross talk with sphingolipid metabolism.

Chrysin attenuates testosterone-induced benign prostate hyperplasia in rats.

Benign prostate hyperplasia (BPH) is a common age-related health problem affecting almost 3 out of 4 men in their sixties. Chrysin is a dietary phytoestrogen found naturally in bee propolis and various plant extracts. It possesses antioxidant, anti-inflammatory and anti-proliferative properties. The current study was conducted to explore the role chrysin plays in protection against testosterone-induced BPH in rats. On grounds of a preliminary experiment, a dose of chrysin (50 mg/kg) was chosen for further investigation. Testosterone significantly depleted glutathione, suppressed superoxide dismutase and catalase activities, and elevated lipid peroxidation. Moreover, it markedly scaled down the level of cleaved caspase-3 enzyme, reduced Bax/Bcl-2 ratio and mRNA expression of p53 and p21; conversely, protein expression of proliferating cell nuclear antigen was enhanced. Chrysin alleviated testosterone-induced oxidative stress and restored cleaved caspase-3 level, Bax/Bcl-2 ratio and mRNA expression of p53 and p21 to almost control levels. Chrysin prevented the increase in binding activity of nuclear factor kappa B (NF-κB) p65 subunit, mRNA expression of insulin-like growth factor 1 (IGF-1) and insulin-like growth factor 1 receptor (IGF-1R). These data highlight the protective role of chrysin against experimentally-induced BPH. This is attributed - at least partly - to its antioxidant, antiproliferative and proapoptotic properties.

Potential neuroprotective effect of androst-5-ene-3ß, 17ß-diol (ADIOL) on the striatum, and substantia nigra in Parkinson's disease rat model.

Parkinson's disease (PD) is a progressive neurodegenerative disorder with behavioral and motor abnormalities. Androst-5-ene-3ß, 17ß-diol (ADIOL), an estrogen receptor (ER) ß agonist, was found to mediate a transrepressive mechanism that selectively modulates the extent of neuroinflammation and, in turn, neurodegeneration. In consensus, ERß polymorphism was more frequently detected in early-onset PD patients. Thus, in an approach to elucidate the role of ERß agonists on PD, our study was designed to investigate the possible neuroprotective effect of ADIOL, in three dose levels (0.35, 3.5, 35 mg/kg/day), against rotenone (ROT)-induced PD rat model. Amelioration in striatal dopamine (DA), nuclear factor-kappa B (NF-κB), and the expression of down-stream inflammatory mediators, as well as apoptotic markers were observed in the striatum and substantia nigra (SN) upon pre-treatment with the three doses of ADIOL. Similarly, light microscopy (LM) examination revealed declined degeneration of neurons upon pretreatment with ADIOL. Significant improvement in nigral tyrosine hydroxylase (TH) and reduction of nigral α-synuclein densities were also detected after ADIOL pre-treatment with better results frequently achieved with the middle dose (3.5 mg/kg/day). The middle dose of ADIOL showed behavioral improvement, with elevation in the ATP level, which was emphasized by the improvement in mitochondrial integrity observed upon electron microscopy (EM) examination. In conclusion, the present study confirmed for the first time the ability of ADIOL to protect against neuroinflammation and, in turn, neurodegeneration process and motor dysfunction in PD animal model, which was more obviously observed with the middle dose.

Effects of genistein on pentylenetetrazole-induced behavioral and neurochemical deficits in ovariectomized rats.

Estrogenic compounds have been documented in literature to exert neuroprotective effects. This study investigated the potential neuroprotective effect of genistein; a phytoestrogen at doses of 5, 10, 20, and 40 mg/kg p.o. in ovariectomized rats challenged with pentylenetetrazole (PTZ) 90 mg/kg i.p. Systemic acute administration of PTZ induced seizures, increased oxidative stress, and caused apoptosis and histological abnormalities. Pretreatment with genistein delayed seizure onset, reduced the seizure duration, improved oxidative stress profile, decreased estrogen receptor expression, reduced apoptosis, and improved the histopathological pattern. Overall, the genistein doses (10 and 20 mg/kg) showed the strongest protective effects. In conclusion, the current study suggests that genistein exhibits neuroprotective effects against PTZ-induced seizures. Such effects might be attributed to its estrogenic, antioxidant, and/or anti-apoptotic properties.

Antioxidant and antiapoptotic actions of selegiline protect against 3-NP-induced neurotoxicity in rats.

The present study was designed to investigate the neuroprotective effect of selegiline on 3-nitropropionic acid (3-NP)-induced neurotoxicity. Selegiline was intraperitoneally injected at doses 2.5, 5, and 10 mg/kg, 3 days prior to and continued daily, 30 min before 3-NP administration. 3-NP (20 mg/kg, i.p.) was administered for four consecutive days. 3-NP-treated rats exhibited PPI deficits, locomotor hypoactivity, increased striatal and cortical lipid peroxidation, and reduced respective glutathione (GSH) levels as well as catalase and superoxide dismutase (SOD) activities. Changes in the level of the apoptotic regulatory gene expressions were demonstrated as increased striatal and cortical caspase-3 and Bax and decreased respective Bcl2. The two higher dose levels of selegiline (5 and 10 mg/kg) significantly increased locomotor activity, improved prepulse inhibition (PPI), reduced striatal and cortical lipid peroxidation, caspase-3, and Bax, and increased GSH level, catalase, and superoxide dismutase activities and Bcl2 expression. Selegiline at dose 2.5 mg/kg could only reverse some of the manifestations of 3-NP-induced neurotoxicity. Histological examination further affirmed the neuroprotective effect of the higher dose levels of selegiline against 3-NP-induced toxicity. Taken together, these results suggest that selegiline could attenuate 3-NP-induced neurotoxicity. This can be attributed to, at least partly, its antioxidant and antiapoptotic effects.

Tetramethylpyrazine Ameliorates Rotenone-Induced Parkinson's Disease in Rats: Involvement of Its Anti-Inflammatory and Anti-Apoptotic Actions.

Parkinson's disease (PD) is a slowly progressive neurodegenerative movement disorder. Apoptosis, neuroinflammation, and oxidative stress are the current hypothesized mechanisms for PD pathogenesis. Tetramethylpyrazine (TMP), the major bioactive component of Ligusticum wallichii Franchat (ChuanXiong), Family Apiaceae, reportedly has anti-apoptotic, anti-inflammatory and antioxidant effects. This study investigated the role of 'TMP' in preventing rotenone-induced neurobiological and behavioral sequelae. A preliminary dose-response study was conducted where rats received TMP (10, 20, and 40 mg/kg, i.p.) concomitantly with rotenone (2 mg/kg, s.c.) for 4 weeks. Catalepsy, locomotor activity, striatal dopamine content, and tyrosine hydroxylase "TH" and α-synuclein immunoreactivity were evaluated. The selected TMP dose (20 mg/kg) was used for western blot analysis of Bax, Bcl2, and DJ-1, immunohistochemical detection of nuclear factor kappa B (NF-кB), inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX2), and glial fibrillary acidic protein (GFAP) expression, in addition to biochemical analysis of caspase-3 activity, nuclear factor erythroid 2-related factor 2 (Nrf2), and heme oxygenase-1 (HO-1) levels. Results showed that TMP (20 mg/kg) significantly improved midbrain and striatal TH expression and striatal dopamine content as well as the motor deficits, compared to rotenone-treated group. These results were correlated with reduction in caspase-3 activity and α-synuclein expression, along with improvement of midbrain and striatal Bax/Bcl2 ratio compared to rotenone-treated group. TMP also attenuated rotenone-induced upregulation of Nrf2/HO-1 pathway. Furthermore, TMP downregulated rotenone-induced neuroinflammation markers: NF-кB, iNOS, COX2, and GFAP expression in both the midbrain and striatum. Taken together, the current study suggests that TMP is entitled to, at least partially, preventing PD neurobiological and behavioral deficits by virtue of its anti-apoptotic, anti-inflammatory, and antioxidant actions.

Novel combination of sorafenib and biochanin-A synergistically enhances the anti-proliferative and pro-apoptotic effects on hepatocellular carcinoma cells.

Sorafenib (SOR) is the first-line treatment for hepatocellular carcinoma (HCC). However, its use is hindered by the recently expressed safety concerns. One approach for reducing SOR toxicity is to use lower doses in combination with other less toxic agents. Biochanin-A (Bio-A), a promising isoflavone, showed selective toxicity to liver cancer cells. We postulated that combining SOR and Bio-A could be synergistically toxic towards HCC cells. We further evaluated the underlying mechanism. Cytotoxicity assay was performed to determine the IC50 of Bio-A and SOR in HepG2, SNU-449 and Huh-7 cells. Then, combination index in HepG2 was evaluated using Calcusyn showing that the concurrent treatment with lower concentrations of SOR and Bio-A synergistically inhibited cell growth. Our combination induced significant arrest in pre-G and G0/G1 cell cycle phases and decrease in cyclin D1 protein level. Concomitantly, SOR/Bio-A reduced Bcl-2/Bax ratio. Furthermore, this co-treatment significantly increased caspase-3 &-9 apoptotic markers, while decreased anti-apoptotic and proliferative markers; survivin and Ki-67, respectively. Active caspase-3 in HepG2, SNU-449 and Huh-7 confirmed our synergism hypothesis. This study introduces a novel combination, where Bio-A synergistically enhanced the anti-proliferative and apoptotic effects of SOR in HCC cells, which could serve as a potential effective regimen for treatment.

Genistein improves sensorimotor gating: Mechanisms related to its neuroprotective effects on the striatum.

Huntington's disease (HD) is a neurodegenerative disorder, characterized by selective atrophy in the striatum, particularly the medium spiny GABAergic efferent neurons. This results in striatal sensorimotor gating deficits. Systemic administration of 3-nitropropionic acid (3-NPA) produces selective lesions mimicking those of HD. Males were found to be more susceptible to 3-NPA-induced neurotoxicity than females, suggesting neuroprotective effects of estrogens. Phytoestrogens, including genistein, are good estrogenic alternatives that keep their beneficial effects on non-reproductive organs and lack the potential hazardous side effects. The current study was designed to investigate the potential beneficial effects of genistein in 3-NPA-induced HD in ovariectomized rats. Results showed that 3-NPA (20 mg/kg) administration caused significant disruption of the rats' locomotor activity and prepulse inhibition. In addition, it decreased striatal ATP levels and increased oxidative stress, inflammatory and apoptotic markers with striatal focal hemorrhage and gliosis. Pretreatment with 17ß-estradiol (2.5 mg/kg) or genistein (20 mg/kg) led to a significant improvement of behavioral parameters, increased ATP production, decreased oxidative stress, attenuated inflammation and apoptosis. Therefore, this study suggests potential neuroprotective effects of genistein in ovariectomized rats challenged with 3-NPA.

Caffeic Acid Phenethyl Ester: A Review of Its Antioxidant Activity, Protective Effects against Ischemia-reperfusion Injury and Drug Adverse Reactions.

Propolis, a honey bee product, has been used in folk medicine for centuries for the treatment of abscesses, canker sores and for wound healing. Caffeic acid phenethyl ester (CAPE) is one of the most extensively investigated active components of propolis which possess many biological activities, including antibacterial, antiviral, antioxidant, anti-inflammatory, and anti-cancer effects. CAPE is a polyphenolic compound characterized by potent antioxidant and cytoprotective activities and protective effects against ischemia-reperfusion (I/R)-induced injury in multiple tissues such as brain, retina, heart, skeletal muscles, testis, ovaries, intestine, colon, and liver. Furthermore, several studies indicated the protective effects of CAPE against chemotherapy-induced adverse drug reactions (ADRs) including several antibiotics (streptomycin, vancomycin, isoniazid, ethambutol) and chemotherapeutic agents (mitomycin, doxorubicin, cisplatin, methotrexate). Due to the broad spectrum of pharmacological activities of CAPE, this review makes a special focus on the recently published data about CAPE antioxidant activity as well as its protective effects against I/R-induced injury and many adverse drug reactions.

ADIOL protects against 3-NP-induced neurotoxicity in rats: Possible impact of its anti-oxidant, anti-inflammatory and anti-apoptotic actions.

Huntington's disease (HD) is a progressive neurodegenerative disorder with a wide spectrum of cognitive, behavioral and motor abnormalities. The mitochondrial toxin 3-nitropropionic acid (3-NP) effectively induces specific behavioral changes and selective striatal lesions similar to that observed in HD. Some neurosteroids, synthesized in neurons and glial cells, previously showed neuroprotective abilities. 5-Androstene-3ß-17ß-diol (ADIOL) is a major metabolite of dehydroepiandrosterone (DHEA) with previously reported anti-inflammatory, anti-apoptotic and neuroprotective activities. The neuroprotective potential of ADIOL in HD was not previously investigated. Therefore, the present study investigated the neuroprotective effects of ADIOL against 3-NP-induced behavioral changes, oxidative stress, inflammation and apoptosis. Intraperitoneal administration of 3-NP (20mg/kg) for 4 consecutive days in rats caused significant loss in body weight, reduced prepulse inhibition (PPI) of acoustic startle response, locomotor hypoactivity with altered cortical/striatal histological structure, increased cortical/striatal oxidative stress, inflammation and apoptosis. Administration of ADIOL (25mg/kg, s.c.) for two days before 3-NP significantly attenuated the reduction in body weights and PPI, increased locomotor activity and restored cortical/striatal histological structure nearly to normal. Moreover, it displayed anti-oxidant, anti-inflammatory and anti-apoptotic activities as evidenced by the elevation of cortical and striatal reduced glutathione levels, reductions of cortical and striatal malondialdehyde, striatal tumor necrosis factor alpha and interleukin-6 levels. Only a small number of iNOS and caspase-3 positive cells were detected in sections from rats pretreated with ADIOL. This study suggests a potential neuroprotective role of ADIOL against 3-NP-induced Huntington's disease-like manifestations. Such neuroprotection can be attributed to its anti-oxidant, anti-inflammatory and anti-apoptotic activities.