<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Amr A Fouad</style></author><author><style face="normal" font="default" size="100%">Entesar F Amin</style></author><author><style face="normal" font="default" size="100%">Amira F Ahmed</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Naringenin and Vanillin Mitigate Cadmium-Induced Pancreatic Injury in Rats via Inhibition of JNK and p38 MAPK Pathways</style></title><secondary-title><style face="normal" font="default" size="100%">Pharmacognosy Journal</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">CdCl2</style></keyword><keyword><style  face="normal" font="default" size="100%">JNK/MAPK</style></keyword><keyword><style  face="normal" font="default" size="100%">Naringenin</style></keyword><keyword><style  face="normal" font="default" size="100%">p38/MAPK</style></keyword><keyword><style  face="normal" font="default" size="100%">Pancreas</style></keyword><keyword><style  face="normal" font="default" size="100%">Vanillin</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2020</style></year><pub-dates><date><style  face="normal" font="default" size="100%">June 2020</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">12</style></volume><pages><style face="normal" font="default" size="100%">742-748</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p class=&quot;rtejustify&quot;&gt;&lt;strong&gt;Background: &lt;/strong&gt;Cadmium can induce pancreatic injury via oxidative stress, inflammation and apoptosis. Naringenin (NGN) and vanillin (VLN) exert antioxidant, anti-inflammatory, and antiapoptotic effects. &lt;strong&gt;Objective: &lt;/strong&gt;The likely ameliorative effects of NGN, VLN and their combination were studied in rats exposed to cadmium-induced pancreatic injury. &lt;strong&gt;Materials and Methods: &lt;/strong&gt;Rats received NGN (50 mg/kg/day, p.o.), VLN (100 mg/ kg/day, p.o.), or NGN + VLN for 7 days and one injection of CdCl&lt;sub&gt;2&lt;/sub&gt; (2 mg/kg, i.p.) on the 6&lt;sup&gt;th&lt;/sup&gt; day. &lt;strong&gt;Results:&lt;/strong&gt; Cadmium significantly lowered serum amylase and insulin levels. Cadmium also caused significant increments of malondialdehyde, tumor necrosis factor-α, interleukin-1β, nuclear factor-κB p65, Bax/Bcl-2 ratio and phosphorylated c-Jun N-terminal kinase (p-JNK) and p38 mitogen-activated protein kinases (MAPKs) and significant decrements of reduced glutathione and catalase in the pancreas of rats received CdCl&lt;sub&gt;2&lt;/sub&gt;. Additionally, CdCl&lt;sub&gt;2&lt;/sub&gt; caused marked histopathological necrosis and significantly increased caspase-3 expression in pancreatic tissue. The cadmium-induced biochemical, histopathological and immunohistochemical changes were significantly ameliorated by NGN, VLN and NGN + VLN. However, NGN + VLN caused more significant ameliorative effects than did NGN and VLN alone. &lt;strong&gt;Conclusion: &lt;/strong&gt;NGN, VLN and NGN + VLN afforded significant protection of pancreas in rats exposed to cadmium insult through modulation of JNK and p38 MAPK pathways and inhibition of oxidative stress, inflammation and apoptosis.&lt;/p&gt;
</style></abstract><issue><style face="normal" font="default" size="100%">4</style></issue><work-type><style face="normal" font="default" size="100%">Original Article</style></work-type><section><style face="normal" font="default" size="100%">742</style></section><auth-address><style face="normal" font="default" size="100%">&lt;p class=&quot;rtejustify&quot;&gt;&lt;strong&gt;Amr A Fouad&lt;sup&gt;1,2,&lt;/sup&gt;*, Entesar F Amin&lt;sup&gt;2&lt;/sup&gt;, Amira F Ahmed&lt;sup&gt;3&lt;/sup&gt;&lt;/strong&gt;&lt;/p&gt;

&lt;p class=&quot;rtejustify&quot;&gt;&lt;sup&gt;1&lt;/sup&gt;Department of Pharmacology, Faculty of Medicine, Al-Baha University, Al-Baha, SAUDI ARABIA.&lt;/p&gt;

&lt;p class=&quot;rtejustify&quot;&gt;&lt;sup&gt;2&lt;/sup&gt;Department of Pharmacology, Faculty of Medicine, Minia University, El-Minia, EGYPT.&lt;/p&gt;

&lt;p class=&quot;rtejustify&quot;&gt;&lt;sup&gt;3&lt;/sup&gt;Department of Histology, Faculty of Medicine, Minia University, El-Minia, EGYPT.&lt;/p&gt;
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