Downregulation of inflammatory erectile dysfunction by Mantisa religiosa egg-cake through NO-cGMP-PKG dependent NF-kB signaling cascade activated by mixture of salt intake.

We hypothesized whether 10% praying-mantis-egg-cake (10% PMEC) can be applied against inflammatory-erectile-dysfunction and whether it could be linked to NO-cGMP-dependent PKG signaling cascade. Ninety male albino-rats were randomly distributed into nine (n = 10) groups. Group I was given distilled water. Group II and III were pre-treated with 80 mg/kg NaCl and 75 mg/kg MSG, respectively. Group IV was pre-treated with 80 mg/kg NaCl + 75 mg/kg MSG. Group V was administered with 80 mg/kg NaCl+ 3 mg/kg Amylopidin. Group VI was given 80 mg/kg NaCl + 10% PMEC. Group VII was treated with 75 mg/kg MSG + 10% PMEC. Group VIII was treated with 80 mg/kg NaCl+ 75 mg/kg MSG + 10% PMEC. Group IX was post-treated with 10% PMEC for 14 days. Penile PDE-51, arginase, ATP hydrolytic, cholinergic, dopaminergic (MAO-A) and adenosinergic (ADA) enzymes were hyperactive on intoxication with NaCl and MSG. The erectile dysfunction caused by inflammation was linked to alteration of NO-cGMP-dependent PKG signaling cascade via up-regulation of key cytokines and chemokine (MCP-1). These lesions were prohibited by protein-rich-cake (10% PMEC). Thus, protein-rich-cake (10% PMEC) by a factor of 4 (25%) inhibited penile cytokines/MCP-1 on exposure to mixture of salt-intake through NO-cGMP-PKG dependent-NF-KB signaling cascade in rats.

Naringin attenuates Bisphenol-A mediated neurotoxicity in hypertensive rats by abrogation of cerebral nucleotide depletion, oxidative damage and neuroinflammation.

We examined whether active fruit naringin can reduce the risk of BPA-mediated neurotoxicity in L-NAME induced hypertensive rats and whether the modulation could be linked to improvement of brain NO signaling. Male albino rats were randomly distributed into eight (n = 7) groups. Group I was control animals, Group II was orally-treated with L-NAME, Group III was orally treated with 100 mg/kg BPA, Group IV was orally-treated with L-NAME +100 mg/kg BPA. Group V was orally-administered with L-NAME +80 mg/kg NAR. Group VI was orally-administered with 100 mg/kg BPA +80 mg/kg NAR. Group VII was orally-administered with L-NAME+100 mg/kg BPA +80 mg/kg NAR. Lastly, group VIII was orally-treated with 80 mg/kg NAR. The treatment lasted for 14 days. Sub-acute exposure to L-NAME and BPA induced hypertension and mediated-neuroinflammation at CA-2 and CA-4 of hippocampus cells. It was evident by increase in PDE-51 and enzymes of ATP hydrolysis (ATPase, ADPase and AMPase) with corresponding upsurge in cholinergic (AChE and BuChE), dopaminergic (MAO-A) and adenosinergic (ADA) enzymes as well as movement disorder. The hypertensive-mediated neurotoxicity was related to alteration of NO signaling and higher release of pro-inflammatory cytokines (TNF-α and IL-1ß), apoptotic proteins (P53 and caspace-9) and facilitated entry of T-lymphocytes (CD43+) into CNS through blood brain barrier potentiated by antigen presenting cells. Hence, these features of BPA-mediated neurotoxicity in L-NAME induced hypertensive rats were prohibited by co-administration of NAR through production of neuro-inflammatory mediators, stabilizing neurotransmitter enzymes, normalizing NO signaling and improving brain histology.

Naringin regulates erectile dysfunction by abolition of apoptosis and inflammation through NOS/cGMP/PKG signalling pathway on exposure to Bisphenol-A in hypertensive rat model.

This study investigated the effect of naringin (NRG) on extracellular metabolism of ATP through the NOS/cGMP/PKG signaling pathway induced by Nω-nitro-L-arginine methyl ester hydrochloride (L-NAME) on exposure to Bisphenol-A (BPA) in penis. Fifty-six adult male albino rats were randomly distributed into eight (n = 7) groups. Group I: control animals, Group II was treated with 40 mg/kg L-NAME, Group III was treated with 50 mg/kg BPA, Group IV was treated with 40 mg/kg L-NAME +50 mg/kg BPA. Group V was administered with 40 mg/kg L-NAME +80 mg/kg NRG. Group VI was administered with 50 mg/kg BPA + 80 mg/kg NRG. Group VII was administered with 40 mg/kg L-NAME+50 mg/kg BPA + 80 mg/kg NRG. Lastly, group VIII was treated with 80 mg/kg NRG for 14 days. NRG prevented hypertension and erectile dysfunction by inhibiting the activities of angiotensin-converting enzymes, arginase, and phosphodiesterase-51 (PDE-51) with corresponding down-regulation of inflammatory markers including TNF-α and IL-B. Additionally, hypertensive erectile dysfunction was remarkably prevented by NRG as manifested by the declined activities of AChE, MAO-A and enzymes of ATP hydrolysis (ATPase, ADPase, AMPase and ADA) with resultant increase in NO level. Also, penile expression of antigen presenting cells, CD43 transcript, caspace-9 and tumor suppressor P53 proteins were repressed on treatment with NRG. This study validates the hypothesis that NRG may be a valuable remedy in abrogating penile inflammatory markers, apoptosis and enzymes of ATP-hydrolysis via NOS/cGMP/PKG signaling pathways in hypertensive rat model on exposure to environmental toxicant.

Naringin protects against Bisphenol-A induced oculopathy as implication of cataract in hypertensive rat model.

People who have experienced high blood pressure are at greater risk of susceptibility to other health problems including oculopathy. The patients with these experiences do not have adequate treatment and those who do; spend much funds on the drug purchase. The study examines the protective effect of naringin (NRG) against ocular impairment in L-NAME induced hypertensive rat on exposure to a cellular disruptor. Fifty-six adult male albino rats were randomly distributed into eight (n = 7) groups. Group I: control animals, Group II was treated with Nω-nitro-L-arginine methyl ester hydrochloride (L-NAME), Group III was treated with 50 mg/kg Bisphenol-A, Group IV was treated with L-NAME +50 mg/kg Bisphenol-A. Group V was administered with L-NAME +80 mg/kg NRG. Group VI was administered with 50 Mg/kg BPA + 80 mg/kg NRG. Group VII was administered with L-NAME+50 mg/kg Bisphenol-A +80 mg/kg NRG. Lastly, group VIII was treated with 80 mg/kg NRG alone for 14 days. Naringin prevented hypertension and ocular dysfunction by depleting the activities of angiotensin-converting enzymes, arginase, aldose-reductase and phosphodiesterase-51 (PDE-51) with corresponding down-regulation of inflammatory markers including TNF-α and IL-B. Moreover, ocular impairment was remarkably reduced by NRG as manifested by the decreased activities of AChE, BuChE, MAO-A and enzymes of ATP hydrolysis (ATPase, ADPase, AMPase) and adenosine deaminase with resultant increased NO level. Also, ocular expression of CD43 transcript, caspaace-9 and tumor suppressor P53 proteins were suppressed on treatment with NRG. This study corroborates the view that NRG may be a useful therapy in alleviating inflammatory markers, apoptosis and metabolic nucleotides disorders via the NOS/cGMP/PKG signaling pathways in hypertensive rat model on exposure to a cellular disruptor.